Worldwide, tuberculosis (TB) affects 10 million people and causes 2 million deaths each year. In developed countries it is uncommon, affecting approximately 1 per 10 000 population. Pulmonary TB is most common in Asian, Chinese and West Indian people. Airborne transmission and close contact spread the disease. Those who are elderly, malnourished or immunosuppressed (HIV infection, diabetes mellitus, corticosteroid therapy, alcoholism, intercurrent lymphoma) are more susceptible. Improved housing and nutrition reduce incidence.
Primary pulmonary TB is caused by the acid-fast bacillus Mycobacterium tuberculosis. The inhaled bacillus infects well-ventilated, poorly perfused upper lung lobes subpleurally. A granuloma forms (Fig. 38a) known as the Ghon focus, and with the enlarged hilar lymph node draining the affected lung is known as the 'primary complex' (Fig. 38a). This occurs over 3-8 weeks, and is accompanied by development of an inflammator reaction to injection of tubercular protein (tuberculin) into the skin, which can be used as a diagnostic test (Mantoux or Heaf test). Complete healing usually follows, with fibrosi and calcificatio of the Ghon focus and immunity to further infection.
Post-primary pulmonary TB occurs if the Ghon focus fails to heal due to poor host defences, or following reactivation. It is potentially fatal. Local dissemination causes tuberculous pneumonia and pleural effusions. Bloodborne spread may affect the meninges or individual organs. In a few cases, widespread infection involves many tissues (miliary TB).
Primary pulmonary TB usually occurs at an early age. Often asymptomatic with no clinical signs, it may cause a mild febrile illness, erythema nodosum (painful, indurated shin lesions) and small pleural effusions. Bronchial compression by lymphadenopathy may cause wheeze and occasionally lobar collapse followed by late bronchiectasis (Chapter 34).
Post-primary TB develops over months, with malaise, anorexia, weight loss, night sweats and a productive cough. Breathlessness, chest pain, haemoptysis and cervical lymphadenopathy may occur. Clinical signs of pneumonia and pleural effusion are common, whereas lupus vulgaris (an indolent skin infection) is less frequent. Miliary TB presents with a non-specifi pyrexial illness, malaise and weight loss. Sparse clinical signs include hepatomegaly and choroidal tubercles in the retina.
Blood tests may detect anaemia, decreased sodium and increased calcium.
Mantoux test: strongly positive in post-primary pulmonary TB (>5 mm skin induration with 10 units of intradermal tuberculin; read at 3 days). Often negative in miliary TB (reduced host response) and HIV (reduced cellular immunity).
Heaf test (screening test; now less commonly used): a ring of six pinpricks is made through a tuberculin solution on the forearm. No response at 4-7 days (grade 0) demonstrates lack of immunity; 4-6 discrete nodules (grade 1) or a ring formed by coalition of all pinpricks (grade 2) indicates immunity. A single nodule formed by infillin of the ring (grade 3) represents recent contact or early tuberculous infection, and a nodule of more than 5-7 mm with surface vesicles or ulceration (grade 4) suggests infection.
Microbiology: the acid-fast bacilli may be detected in sputum or lung washings using Ziehl-Neelsen stain. However, bacilli are slow growing, and culture and drug sensitivities take 4-6 weeks. Bone marrow or cerebrospinal f uid (CSF) culture may confir the diagnosis of miliary TB.
Histopathology: pleural aspiration with biopsy confirm TB in ap- proximately 90% of patients with pleural effusions. Liver biopsy will isolate miliary TB in approximately 60% of cases.
Chest radiography (Fig. 38b): upper lobe shadowing is suggestive. Apical cavities, pleural effusions and pneumothoraxes may occur. In miliary TB, widespread small nodules (2-3 mm diameter) are diffusely spread throughout the lungs (miliary shadowing), and are easily missed.
Prognosis is good if the patient is not immunocompromised. Good nutrition, reduced alcohol consumption and compliance with drug therapy are important factors. Uncomplicated pulmonary TB is treated for 6 months. Initially, at least three drugs are used to prevent development of resistant strains. The recommended regimen is rifampicin, pyrazinamide and isoniazid for 2 months, followed by rifampicin and isoniazid for 4 months. Additional pyridoxine prevents isoniazid-induced peripheral neuropathy. Liver function should be monitored, as rifampicin and pyrazinamide can cause liver dysfunction. If drug resistance is suspected (TB recurrence in a non-compliant patient) then a four-drug regimen (adding ethambutol) may be initiated. When culture results are available, alternative drugs replace those to which the mycobacterium is not sensitive. Ethambutol (monitor colour vision for optic neuritis), streptomycin (monitor plasma levels to avoid hearing impairment) or ciprofloxaci may be used. In severe pulmonary TB, corticosteroids occasionally improve results.
In some organs (e.g. bone), TB is treated for longer, often with additional drugs. In meningeal or cerebral TB, a four-drug regimen for 12 months with additional steroids is recommended, to ensure adequate brain penetration and to prevent cranial nerve compression by meningeal scarring.
Reactivation of old tuberculous scars may occur when a patient is immunocompromised (Fig. 38c). Chemoprophylaxis with isoniazid is often given before immunosuppressive treatment (chemotherapy, organ transplantation). Bronchiectasis and lung cavities with secondary fungal infections (mycetoma), cranial nerve lesions and renal tract obstructions may develop due to scarring associated with healing after TB. Non-compliance or inadequate treatment results in multiresistant strains of mycobacteria that may be very difficul to eradicate. Compulsory supervision and isolation of these patients may be required.
Prevention and contact tracing
Vaccination of non-immune subjects with BCG (bacille Calmette-Gue'rin), a non-virulent strain of bovine TB, produces immunity and reduces the risk of pulmonary TB by 70%. Community health services must be notiﬁed when a patient is diagnosed with TB, to trace contacts and prevent spread. Contacts are screened with a Mantoux test. If this suggests a risk of infection, then chest and appropriate follow-up are arranged.
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