Pathogenesis and pathology
First infection of the lung with the tubercle bacillus is known as primary pulmonary tuberculosis. This occurs from inhalation of the bacillus, which gets deposited in an alveolus. From this primary site of infection, bacilli are carried to the lymph nodes via lymphatics, and the hilar nodes enlarge. This parenchymal lesion (Ghon's lesion) with its enlarged regional (hilar) lymph nodes and interconnecting lymphangitis is known as the primary complex of Ranke (Ghon's complex).
The parenchymal lesion is subpleural and is usually located in lower part of the upper lobe, upper part of the lower lobe or the middle lobe. After about 3-8 weeks of infection (by the time of tuberculin conversion), the classical pathological features of tuberculosis may be found in varying proportions. This is a granulomatous lesion containing epithelioid cells derived from macrophages, Langhans' giant cells with multiple nuclei also derived from macrophages, lymphocytes and varying degrees of fibrosis. Later, a peculiar cheesy form of necrosis occurs in the centre, known as caseation. The caseous tissue may later become calcified. But if the lesion progresses, the caseous tissue may become liquefied to form purulent material. This material may be discharged into a bronchus resulting in cavitation of the lesion. Cavitation, however, is regarded as one of the manifestations of post-primary pulmonary tuberculosis.
The pathological changes in the lymph nodes are similar to that of the parenchymal lesion.
Primary infection usually occurs in childhood. A history of contact with a case of active tuberculosis is present in many cases.
Vast majority are asymptomatic.
A minority may experience a brief 'flu-like' febrile illness, which lasts no more than 7-14 days. It occurs at the time of tuberculin conversion.
If the infection is severe or the host resistance is low, child may appear to be vaguely unwell with reduced appetite, fretfulness and failure to gain weight.
Slight dry cough is occasionally present. Wheeze may be rarely present.
In vast majority, there are no abnormal physical signs.
When the lesion is severe or extensive, signs of general debility may be present. Child is thin, pale and fretful with less glossy hair and less elastic skin.
Usually there are no abnormal physical signs in the chest. Sometimes, there may be a few crepitations over a large
lung component of the primary complex. More extensive physical signs in the chest result from complications.
Erythema nodosum may accompany primary pulmonary tuberculosis. These are bluish-red, raised, tender, cutaneous lesions on the shins and less commonly on the thighs. In some patients, it is associated with fever and polyarthralgia. Tuberculin reaction is strongly positive in this group. Erythema nodosum is also seen in other conditions like sarcoidosis, streptococcal infections and drug reactions.
Symptoms and signs may result from progression of primary complex or complications of primary complex (refer 'fate of primary complex').
Fate of the primary complex
In great majority, the primary focus heals completely with or without calcification.
In some cases, the primary focus is walled off by collagenous tissue, the tubercle bacilli cease to divide and the disease becomes dormant. However, these dormant lesions can reactivate later giving rise to active post-primary pulmonary tuberculosis.
In a few individuals, primary lesion in the lung may be actively progressive from the beginning (progressive pulmonary tuberculosis or progressive primary pulmonary tuberculosis).
In a few cases, healing, particularly in lymph nodes, is incomplete and viable tubercle bacilli may enter the bloodstream. As a result, haematogenous dissemination occurs resulting in tuberculous lesions elsewhere. The haematogenous forms can be of two types:
The acute form, which is more likely to occur in infants or young children, results in miliary tuberculosis or tuberculous meningitis.
The chronic form, where tuberculous lesions develop in the lungs, bones, joints and kidneys. These lesions may develop months or even years after primary infection.
In some cases, the infection may be carried by lymphatics from mediastinal lymph nodes to pleura or pericardium resulting in tuberculous pleurisy with effusion or tuberculous pericarditis with effusion.
Bronchial complications resulting from primary complex are the following:
Enlarged mediastinal lymph nodes can compress a bronchus resulting in pulmonary collapse. Compression of middle lobe bronchus is especially common, leading to collapse-consolidation and bronchiectatic changes. This may present later as the 'middle lobe syndrome'.
Tuberculous lymph node may ulcerate through the bronchial wall and discharge caseous material into the lumen. This results in bronchial spread to the related lobe or segment.
Rarely, the bronchus is so compressed as to result in a valve action with air trapping. This leads to obstructive emphysema.
Calcification in a primary focus or lymph node may later be extruded into a bronchus as a 'broncholith', presenting as haemoptysis.
History of contact with a case of active tuberculosis.
Tuberculin test is very valuable in children. A positive test in a previously non-immunised child strongly indicates the disease. A negative test makes the diagnosis very unlikely.
Chest radiograph can visualise the primary complex as a peripheral parenchymal lesion and an enlarged hilar lymph node.
In children, glandular component (enlarged hilar lymph node) of the complex is more obvious than the pulmonary component.
In adults, pulmonary component (peripheral parenchymal lesion) of the complex is more obvious than the glandular component.
Sputum examination is preferable, but it is seldom available. Alternatively, three laryngeal swabs or fasting gastric washings can be examined.
Isolation of the tubercle bacilli by direct smear examination or culture confirms the diagnosis.