PEDIATRIC TB

Dr. Preethi Subramanian

Asst. Professor
OVERVIEW
• Introduction
• Pathophysiology
• Clinical presentation
• Diagnosis
• Treatment
• Prevention
When Is World TB Day observed
every year?
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
• 70% of Primary foci SUBPLEURAL ‐ sluggish air current in lung
periphery allow bacilli to stay longer.
• Hallmark of primary tuberculosis infection – relatively large size of
adenitis, compared to relatively insignificant size of initial focus in the
lung.
• Right focus is common – greater volume & right bronchus is vertical,
short & wide.
CLINICAL PRESENTATIONS
Intrathoracic
• Pulmonary
• Latent tuberculosis infection
• Primary pulmonary complex
• Progressive primary disease
• Endobronchial tuberculosis
• Miliary tuberculosis
PRIMARY PULMONARY COMPLEX
• Frequently encountered presentation in out patient.
• Mild constitutional symptoms – mild fever, weight loss, anorexia,
decreased activity, irritating dry cough due to enlarged node
compressing bronchi and trachea.
• Implantation site ‐> lymphatics ‐> regional lymph nodes.
• Primary complex‐ lesion at primary site of involvement, draining
lymphatics and inflamed regional LN.
A B

A and B, Posteroanterior and lateral chest radiograph images of an adolescent

showing a 7 mm calcified granuloma in the left lower lobe (arrows).
Right-sided hilar lymphadenopathy
and collapse consolidation lesions
of primary tuberculosis in a 4 yr
old child.
PROGRESSIVE PULMONARY DISEASE
• Complication of primary pulmonary complex.
• Reactivation due to old age, malnutrition, malignant disease, HIV
infection& AIDS, use of immunosuppressive drugs, intercurrent infections.
• Progressive primary TB due to extension of inflammatory process i.e.,
consolidation of lung called galloping consumption or pneumonia alba.
• Caseation necrosis ‐> liquefaction ‐> cavity.
• Tuberculous cavities are site of growth of bacilli due to optimal
temperature, more O2 content and nutrients from cell wall available
• Cavitary disease uncommon in children.
• It primarily involves apical and posterior segment of upper lobes or
superior segment of lower lobes in <95% cases.
• Enlarged paratracheal nodes cause stridor or RD.
• Subcarinal nodes on esophagus cause dysphagia.
• Complete bronchial obstruction cause atelectasis.
• Seeding of apex of lung leads to development of Simon's focus.
• Endogenous reactivation of apex of lung is Pulh’s leison
ENDOBRONCHIAL TB
• Fever & trouble some cough (with or without sputum).
• Dyspnea, wheezing and cyanosis.
• Misdiagnosed as asthma.
• Wheezing child < 2 years if there is poor response to anti–asthma
medications should raise suspicion.
• Partial airway compression – emphysema.
• Complete airway compression ‐ collapse.
Posteroanterior (A) and lateral (B) chest radiographs of an infant with miliary tuberculosis. The child’s
mother had failed to complete treatment for pulmonary tuberculosis twice within 3 yr of this child’s birth.
MILIARY TB
• Heavy hematogenous spread causing disease in 2 or more organs ‐ Innumerable
small foci.
• Miliary tuberculosis usually complicates the primary infection, occurring within 2-
6 mo of the initial infection.
• Common in infants and malnourished or immunosuppressed patients.
• Symptoms depend on bacillary load & organs involved.
• Lesions are often larger and more numerous in the lungs, spleen, liver, and bone
marrow than other tissues.
• High fever, rigors, altered sensorium, meningitis, lymphadenopathy &
hepatosplenomegaly.
• Smaller than 2‐3 mm in diameter ‐ coalesce to form larger lesions.
• 40% are TST negative.
Pleural TB in an adolescent Girl
TB PLEURAL EFFUSION
• Rupture of subpleural focus result in pleural effusion due to
hypersensitivity of tubercular proteins.
• Tuberculous pleural effusion‐ uncommon in children below 5yrs,more
common in boys and rarely associated with segmental leison or
miliary TB.
• Early stages‐pleural rub, decreased chest wall movements, impairment
of percussion note, decreased air entry on affected
CLINICAL PRESENTATION
Extrathoracic
• Most common forms‐ peripheral lymphadenopathy & CNS
• Osteoarticular
• Abdominal/GIT
• Cardiovascular
• Genitourinary
• Cutaneous and
• Congenital TB
TB LYMPHADENITIS
• Most common form of Extrapulmonary TB.
• 8-10% incidence.
• From drinking unpasteurized cow milk or extension of primary lesion.
• Supraclavicular, tonsillar, submandibular lymph nodes(scrofula)
• Untreated lymphadenitis, caseation necrosis, capsular rupture, spread
to adjacent nodes and skin‐ draining sinus tract.
STAGES OF TB LYMPH NODE
• Stage 1‐enlarged,firm,MOBILE,DISCRETE.
• Stage2‐ large, rubbery, FIXED.
• Stage3‐central softening due to abscess formation.
• Stage 4‐collar stud abscess.
• Stage5‐sinus tract formation.
TB GIT
CNS TB
• The 1st stage typically lasts 1-2 wk and is characterized by nonspecific
symptoms such as fever, headache, irritability, drowsiness, and malaise.
Focal neurologic signs are absent, but infants can experiencea stagnation
or loss of developmental milestones.
• The 2nd stage usually begins more abruptly. The most common features
are lethargy, nuchal rigidity, seizures, positive Kernig and Brudzinski
signs, hypertonia, vomiting, cranial nerve palsies, and other focal
neurologic signs. The accelerating clinical illness usually correlates with
the development of hydrocephalus, increased intracranial pressure,
and vasculitis.
• The 3rd stage is marked by coma, hemi- or paraplegia, hypertension,
decerebrate posturing, deterioration of vital signs, and eventually death.
MRI Brain showing Tuberculomas
as Ring Enhancing Lesions.
PERICARDIAL TB
• 0.5-4% of tuberculosis cases in children.
• Direct invasion or lymphatic drainage from subcarinal lymph nodes.
• The presenting symptoms are nonspecific, including low-grade fever,
malaise, and weight loss. Chest pain is unusual in children.
• A pericardial friction rub or distant heart sounds with pulsus
paradoxus may be present.
• The pericardial fluid is typically serofibrinous or hemorrhagic.
LATENT TB INFECTION
• Reactive tuberculin skin test (TST) + absence of clinical and
radiographic manifestations.
• Infants with Latent TB Infection have up to 40% likelihood of
developing disease.
• But the risk for progression decreases gradually through childhood.
• The greatest risk for progression occurs in the first 2 yr after infection.
RISK FACTORS FOR PROGRESSION OF LATENT
TUBERCULOSIS INFECTION TO TUBERCULOSIS DISEASE

• Infants and children ≤4 yr of age, especially those <2 yr of age

• Adolescents and young adults
• Persons coinfected with HIV
• Persons with skin test conversion in the past 1-2 yr
• Persons who are immunocompromised, especially in cases of
malignancy and solid organ transplantation, immunosuppressive
medical treatments including anti–tumor necrosis factor therapies,
diabetes mellitus, chronic renal failure, silicosis, and malnutrition
INVESTIGATIONS
• Direct evidence
– Bacteriological examination for isolation of bacilli
– Histopathology
– Molecular diagnosis: PCR, Nucleic Acid Probes.
• Indirect evidence
– Biochemical markers
– Immunological techniques
– Supportive investigations – Tuberculin test, BCG test
– Blood examination
– Radiology
– Family screening
• SPECIMENS
• ZN stain
• Auramine –Rhodamine stain
• CULTURE MEDIA
• BACTEC
• Septicheck : modified middle-brook broth used
• Rapid slide culture method
• Mycobacterium growth inhibitor tubes
BIOCHEMICAL MARKERS
• Adenosine deaminase (ADA) –
– level co–relates with proliferation and differentiation of
lymphocytes.
– Normal levels – 13 – 60 units / ml
• Bromide partition test – CSF bromide levels < 1.6 indicates
tuberculous meningitis.
INTERFERON Ɣ RELEASE ASSAYS
• Two blood tests (T-SPOT.TB and QuantiFERON-TB) detect IFN-γ generation by
the patient’s T cells in response to specific M. tuberculosis antigens (ESAT-6,
CFP-10, and TB7.7).
• The QuantiFERON-TB test measures whole blood concentrations of IFN-γ, and
the T-SPOT.TB test measures the number of lymphocytes/monocytes producing
IFN- γ.
• The test antigens are not present on M. bovis–BCG and Mycobacterium avium
complex, the major group of environmental mycobacteria, so one would expect
higher specificity compared with the TST and fewer false-positive results.
IMMUNODIAGNOSIS
• Antibody detection
– Antibodies to crude antigen/ specific antigen (35KDa, P 64, P 32,
38 KDa etc.)
• Antigen detection
– Protein antigens : using polyclonal antibodies / monoclonal
antibodies
– ELISA / RIA test used.
MANTOUX TEST
CSF ANALYSIS
Macroscopy – fluid will be opalescent and on
standing a cob web coagulum
• Cytology
– cell count – 60 – 400 cell / cu.mm,
– early – polymorphs,
– late – mononuclear cells
• Biochemistry –
– protein – > 40 mg / dl,
– sugar – low absent or normal,
– chlorides ‐ < 600
• Microbiology – tuberculosis bacilli may present
DEFINITIONS (DOTS)
• New case ‐ Patient who had not taken ATT previously or has taken for
less than 4 weeks.
• Relapse ‐ Patient declared cured/completed therapy in past and has
evidence of recurrence.
• Treatment after default ‐ A patient who has taken treatment for at
least 4 weeks and comes after interruption of treatment for 2 months
and has active disease.
DEFINITIONS CONTD…
• Failure to respond
A case of pediatric tuberculosis who fails to have bacteriological
conversion to negative status or fails to respond clinically and /or
deteriorates after12weeks of compliant intensive phase shall be deemed
to have failed to respond.
TREATMENT
Use Of Steroids
Can Steroids be used in TB?
PREVENTION
• BCG VACCINE