Pulmonary Tuberculosis (1) by Lecturer of chest diseases Ainshams university http://telemed.shams.edu.eg/moodle5 At the end of this lecture the student should be able to: 1. Describe the pathogenesis, bacteriology, mode of transmission and prevention. 2. Know the clinical presentation (including extra-pulmonary tuberculosis) 3. Interpret the specific investigations. 4. Discuss the BCG vaccination and tuberculin skin testing: indications, technique, value and complications. 5. Discuss the anti-mycobacterial drug regimens including type of drugs, doses, common side effects and duration of therapy as well as methods of follow up (including directly observed therapy) Etiology: Mycobacterium tuberculosis (Koch’s bacillus) is a resistant acid fast and alcohol fast bacillus. Three types can infect man: • The human type: the commonest type. • The bovine type. • The atypical or opportunistic mycobacteria (in AIDS & immunosuppressed patients). Mode of infection: The disease is transmitted through inhalation of infected sputum droplets or ingestion of infected milk. Immunity and Susceptibility: Entry of tubercle bacilli into the body by the respiratory or the alimentary tract is not necessarily followed by a clinical disease, the development of which is dependent on: • Natural resistance: Negroes are more susceptible. • Acquired immunity (BCG vaccination). • Allergy: after the 1ry infection has become established or after BCG vaccination, the tissue reaction to tubercle bacilli takes the form of a hypersensitivity reaction as manifested by a +ve tuberculin reaction caseation in the site of lesion & in the regional LNs. • Age and sex. • Standard of living (increased incidence with poverty due to malnutrition). • Occupation (certain occupations predisposes to tuberculosis as silicosis). • HIV infection leads to reactivation of a preexisting tuberculous infection. Pathology: • • The characteristic lesion of TB is the Tubercle. It consists of a collection of epithelioid cells surrounded by lymphocytes, fibroblasts and giant cells with bacilli in the center. • Adjacent tubercles coalesce central caseation. • The lesions tend to heal by fibrosis & calcification. • The primary TB infection usually occurs in the lung but occasionally in the tonsils or in the alimentary tract accompanied by caseous lesions in the regional lymph nodes: mediastinal, cervical or mesenteric groups respectively. Characteristics of 1ry TB lung lesion (primary complex): • Usually in the lower part of the upper lobe or in the upper part of the lower lobe commonly on right side (Ghon’s focus). • Coexisting endobronchitis and lymphangitis. • Large component of caseous lymph nodes. Stigmata of primary TB infection: • A positive tuberculin test. • Calcified foci in lung and hilar lymph nodes on chest x-ray. Fate of the primary infection: • Usually healing by fibrosis and calcification. Rarely healing is incomplete (due to low general resistance) leading to: • – Hematogenous spread which may lead to: • • Acute military tuberculosis when a lymph node ruptures into a vein. Chronic dissemination leading to tuberculous lesions in lungs, bones, joints and kidneys. Such lesions may develop active tuberculosis months or years after the primary infection. – Progressive pulmonary tuberculosis with primary cavity formation. – A mediastinal lymph node, especially in children, may compress a lung lobe or segment producing pulmonary collapse or may rupture into a bronchus producing acute tuberculous lesions in the related lobe or lung. Postprimary TB may occur: • Directly from a 1ry lesion or • Following reactivation of incompletely healed 1ry focus in the lung or • As a result of Hematogenous dissemination from an unhealed lymph node lesion or • As a result of reinfection from an outside source after the 1ry focus has healed completely. Pathological feature of post-1ry TB: -TB cavity, which forms when the caseated center of a TB lesion is discharged into a bronchus. According to the balance between host resistance and virulence of the organism. Fate of postprimary tuberculosis: • Fibrocaseous TB (commonest type) where cavitation & caseation occur with limited fibrosis. • Acute TB bronchopneumonia when the resistance is low. • Fibrotic tuberculosis (corticopleural type) if the resistance is high. • Extension of infection into the pleura either by direct or lymphatic spread causes TB pleurisy, which is accompanied by effusion and sometimes with TB empyema. (TB pleural effusion is diagnosed by exclusion of other causes of pleural effusion and by its high lymphocyte content and increased levels of ADA). Clinical Features: • Those due to the systemic effects of the disease as malaise, loss of appetite, loss of weight, anemia and pyrexia. • Those caused by local effects of TB lesions: – Lungs and bronchi: cough, sputum, hemoptysis and dyspnea. – Pleura: pleural pain &dyspnea due to pleural effusion. – Larynx: hoarseness of voice. – Tongue: ulceration. – Intestine: diarrhea, malabsorption syndrome or intestinal obstruction. – Peritoneum: ascites and intestinal obstruction due to adhesions. – Pericardium: pericardial effusion and constrictive pericarditis later. – – – – – – – – – – Kidneys and bladder: heamturia, increased frequency of micturition. Fallopian tubes: infertility and tubal abscess. Epididymo-orchitis: painless swelling and later sinus formation. Brain: tuberculoma with or without focal neurological lesions. Meninges: symptoms and signs of meningitis. Lymph nodes: enlargement with cold abscess and sinus formation. Adrenal glands: symptoms and signs of Addison’s disease. Bones and joints: osteitis, synovitis and cold abscesses. Skin: lupus vulgaris and erythema nodosum. Eye: phlyctenular keratoconjunctivitis, iridiocyclitis and choroiditis POSTPRIMARY PULMONARY TB • It is the commonest type of pulmonary TB • It is usually present in upper lobes and is often bilateral as it starts in one lung and spreads via bronchi to other lung. • Occasionally, when the disease takes an acute form, the initial lesion is a pneumonic consolidation. Clinical Features: • Insidious onset & Gradual course • General symptoms • Cough and expectoration, sometimes hemoptysis (blood streaked or frank), • Pleuritic pain (dry pleurisy) or spontaneous pneumothorax marks the onset of the disease, • Later: dyspnea; unless spontaneous pneumothorax or pleural effusion occurs. • Physical signs in chest include medium or coarse crepitations on one or both lung apices posteriorly may be present only after coughing (posttussive crepitations), • Later on: physical signs of consolidation, cavitation and fibrosis may appear. Pleural effusion and pneumothorax may modify the pulmonary signs if present. Differential Diagnosis: • • • • Pneumonia. Bronchial carcinoma. Bronchiectasis. Chronic bronchitis. Complications: • Pleurisy with or without effusion. • Spontaneous pneumothorax, TB empyema or pyopneumothorax. • Tuberculous laryngitis. • Dissemination of tuberculosis. • Ventilatory failure and cor pulmonale. Diagnosis: • Pulmonary tuberculosis should be suspected in cases of: – – – – – Unexplained cough persisting for > two weeks. Hemoptysis. Pleural pain not associated with acute illness. Idiopathic spontaneous pneumothorax. Unexplained tiredness or loss of weight. • The presence of any of these symptoms demand immediate CXR if any abnormality direct examination of at least 3 sputum specimens for acid fast bacilli by ZN stain should be done. • If no sputum can be obtained, bronchial lavage is done through fiberoptic bronchospcopy with direct microscopic examination of the lavaged fluid for acid-fast bacilli, examination by PCR or culture. Pulmonary tuberculosis must be regarded as active and requiring treatment if: • - Local or general symptoms especially hemoptysis or pleural pain. – A radiological opacity known or suspected to be of recent development or of increased extent. – Radiological evidence of cavitation. – Presence of tubercle bacilli in sputum, gastric juice or laryngeal swabs. • X-ray chest usually reveals: 1. ill-defined opacity or opacities situated in one or both upper lobes. 2. Occasionally there is a dense area of consolidation “tuberculous pneumonia”. 3. With advance of the disease cavitation occurs. 4. If there is tendency to healing the opacities shrink and later may show calcification. 5. When fibrosis is marked the trachea and mediastinum are displaced towards the site of the lesion. 6. Occasionally the radiological evidence of pleural effusion or pneumothorax is present.
