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TUBERCULOSIS in Children Gatmaitan, Raymond Golpeo, Kirsten Hemedes, Marielisse.

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Presentation on theme: "TUBERCULOSIS in Children Gatmaitan, Raymond Golpeo, Kirsten Hemedes, Marielisse."— Presentation transcript:

1 TUBERCULOSIS in Children Gatmaitan, Raymond Golpeo, Kirsten Hemedes, Marielisse

2 Pathophysiology Pathophysiology of tuberculosis: inhalation of bacilli, containment in a granuloma, and breakdown of the granuloma in less immunocompetent individuals.

3 Pathophysiology Once inhaled, the infectious droplets settle throughout the airways. The majority of the bacilli are trapped in the upper parts of the airways in the goblet cells. The mucus produced catches foreign substances, and the cilia on the surface of the cells constantly beat the mucus and its entrapped particles upward for removal. Bacteria in droplets that bypass the mucociliary system and reach the alveoli are quickly surrounded and engulfed by alveolar macrophages which destroys the invading mycobacteria and prevent infection. The mycobacteria continue to multiply slowly within the macrophages, with bacterial cell division occuring every 25 to 32 weeks.

4 Pathophysiology Released cytokines attract T lymphocytes to the site, the cells that constitute cell-mediated immunity. Macrophages then present mycobacterial antigens on their surface to the T cells and this process continue for 2 to 12 weeks. For healthy individuals: granuloma formation which destroys macrophages and produce central necrosis (caseous ) but organism tend to survive. By 2 or 3 weeks, caseous necrosis occurs, and is characterized by low oxygen levels, low pH, and limited nutrients. This condition restricts further growth and establishes latency. Lesions in persons with an adequate immune system generally undergo fibrosis and calcification, successfully controlling the infection so that the bacilli are contained in the dormant, healed lesions

5 Pathophysiology The primary complex of tuberculosis includes local infection at the portal of entry and the regional lymph nodes that drain that area. The lung is the portal of ENTRY in >98% of all cases (Inhalation of the bacilli) and hilar lymph nodes are usually involved. The tubercle bacilli multiply initially within alveoli and alveolar ducts Most of the bacilli are killed but some within nonactivated macrophages carry them through lymphatic vessels and regional lymph nodes Tissue reaction in the lung parenchyma and LN intensifies over the next 2 – 12 weeks as the organism grows in number and tissue hypersensitivity occurs. When this portion enlarges it results in focal pneumonitis and pleuritis. Development of fibrosis and encapsulation. During primary complex tubercle bacilli are carried to most tissue of the body through the blood and lymphatic vessels and bacterial replication is more common in places that favor their growth (lung apices, brain, kidneys and bones). Significant LN appears 3 to 9 months. Lesions of the bones and joints take several years and decades for renal lesion.

6 Mode of Transmission Inhalation of droplets Direct contamination of open wounds

7 Period of Communicability Communicable only associated with open lesions of PTB, draining sinuses or renal involvement As long as tubercle bacilli are found in sputum, exudates or urine Children with active primary tuberculosis are rarely contagious (low bacteria output) A patient is non-infectious within 2 to 4 weeks starting adequate therapy

8 Risk factors Age (infants and adoloscents) Close contact with untreated sputum positive patient Impaired host defenses or immunocompromised Person with chest xray sand tuberculin test is suggestive of TB

9 Incubation period From the organism enters the body until cutaneous sensitivity develoop in 3 weeks to 3 months. The end of the incubation period coincides with the onset of tuberculin hypersensitivity Onset of tuberculin hypersensitivity may be accompanied by fever that last for 1 to 3 weeks (fever of onset or invasion).

10 Diagnosis of TB (3 out of 5) 1. Epidemiology 2. Clinical Manifestation Fever and cough of2 weeks or more; poor weight gain; difficulty to recover from a vague, mild illness 3. Radiologic Findings Enlarged LN, hilar adenopathy Pleural effusion on the side of the primary parenchymal lesion 4. Immunologic Tuberculin reaction 5. Laboratory Acid fast staining; cullture, PCR, histopathology

11 TST Recommendation for Infants 1. Children whom immediate TST is indicated: Contacts of people confirmed or suspected contagioius TB Children with radiographic of clinical findings of TB Children immigrating from countries with endemic infection Children with travel histories to countries with endemic infection and substantial contact with indigenous people from such country 2. Children who should have annual TST: Children infected with HIV Children at increased risk for progression of TB (ex. Children with medical condition like DM, malnutrition, chronic renal failure, congenital or acquired immunodeficiency

12 Classification and Diagnosis of Childhood TB 1. CLASS I: TB exposure but (-) Tuberculin test, no signs and symptoms and (-) chest x-ray. 2. CLASS II: TB infection with (+) exposure, (+) Tuberculin Test, no signs and symptoms and (-) chest xray. 3. CLASS III: TB Disease. (A child who has TB has 3 or more of the ff:) (+) exposure (+) Mantoux test Signs and symptoms (+) chest xray Lab findings 4. CLASS IV: TB Inactive With or without (+) exposure With or without previous exposure Has chest xray evidence of healed of calcified TB (+)Mantaoux test Signs and symptoms (-) Smear or culture of TB

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