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
tuberculosis
Mode of Spread:
Inhalation
Ingestion
Penetration of skin and mucous membrane
Predisposing 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
 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
• Primary focus can spread to contiguous part of the lungs
giving rise to tuberculous pneumonia.
• Primary focus and the regional lymph nodes may merge and
give rise to an area of consolidation.
• Extensive caseation and liquefaction can develop giving rise
to cavity formation.
• The inflamed nodes may compress the neighbouring bronchi
giving rise to atelectasis or emphysema.
• Node may erode through the bronchial wall causing
endobronchial tuberculosis.
• There may be discharge of the tubercle bacilli into the lumen
leading to bronchogenic dissemination to other areas of the
lungs.
• Nodes may erode into the blood vessels giving rise to
haematogenous spread to other tissue.
• The affected nodes may develop fibrosis and encapsulation
 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
 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 vague

Chronic cough
Fever
Anorexia
Weight loss
Failure to gain weight
Haemoptysis
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

INVESTIGATIONS
 Tuberculin skin test
 Chest radiograph
 Hilar adenopathy
 Parenchymal lesions
- Patchy infiltrates
- Consolidations
- Atelectasis
- Pleural effusion
- Cavities
17. Bacteriological investigations
- Sputum ) staining
- Gastric washings ) and culture
4. ESR
5. 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 loss
Chest pain on deep inspiration
Signs: Dullness to percussion
Diminished 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
Anorexia
Weight loss
Cough
Wheezing
Signs: Generalised lymphadenopathy.
Hepato-splenomegaly.
Respiratory distress
signs of meningitis or peritonitis present in 20-
40% of cases.
Choroidal tubercles.
 INVESTIGATIONS

Tuberculin skin test

CXR
CSF tap
Histological examination of
Lymph node
Liver biopsy
Marrow 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 stages
Stage I:
Non-specific symptoms like:
Fever
Headache
weight loss
Irritability
Drowsiness
 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

• Tuberculin skin test

• CXR
• 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 good
Stage 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 MANIFESTATION
Headache
Fever
Convulsion
Lateralizing signs
Investigations
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.