Except for the rare intestinal (bovine) tuberculosis and the even more uncommon skin, oropharyngeal, and lymphoidal primary sites, the lungs are the usual location of primary infections. As detailed earlier , the initial focus of primary infection is the Ghon complex, which consists of
a parenchymal subpleural lesion, often just above or just below the interlobar fissure between the upper and the lower lobes, and
enlarged caseous lymph nodes draining the parenchymal focus.
Primary TB can also present as a lower lobe pneumonia. The course and fate of this initial infection is variable, but in most cases patients are asymptomatic, and the lesions undergo fibrosis and calcification.
Exceptionally, particularly in infants and children or immunodeficient adults, progressive spread with cavitation, tuberculous pneumonia, or miliary tuberculosis may follow a primary infection.
Secondary (Reactivation) Pulmonary Tuberculosis
Most cases of secondary pulmonary tuberculosis represent reactivation of an old, possibly subclinical infection. During primary infection, bacilli may disseminate, without producing symptoms, and establish themselves in sites with high oxygen tension, particularly the lung apices. Reactivation in such sites occurs in no more than 5 to 10% of the cases of primary infection. Secondary tuberculosis, however, tends to produce more damage to the lungs than does primary tuberculosis
The subsequent course of the secondary lesions is variable. They either may heal spontaneously, result in a fibrocalcific nodule (with therapy), or progress along the many pathways, discussed next.
Progressive Pulmonary Tuberculosis
A variable number of active lesions continue to progress over a period of months or years, causing further pulmonary and even distant organ involvement. The resultant clinicopathologic consequences include
cavitary fibrocaseous tuberculosis (apical and advanced)
Cavitary Fibrocaseous Tuberculosi
The name fairly well describes this stage of disease. By erosion into a bronchiole, drainage of the caseous focus transforms it into a cavity. Growth and multiplication of the tubercle bacilli under these conditions are favored by the increased oxygen tension. In most cases, the cavity remains localized to the apex (apical cavitary fibrocaseous tuberculosis). The cavity is lined by a yellow-gray caseous material and is more or less walled off by fibrous tissue.
Not uncommonly, thrombosed arteries may traverse these cavities to produce apparent fibrous bridging bands. When such cavitation occurs in the apices, the pathways for further dissemination of the tuberculous infection are prepared. The infective material may now disseminate through the airways to other sites in the lung or upper respiratory tract. Spread may also occur to the lymph nodes via the lymphatics, then retrogressively through other lymphatics to other areas of the lung or other organs. Miliary dissemination through the blood is a further hazard.
Cavitary fibrocaseous tuberculosis may affect one, many, or all lobes of both lungs in the form of
isolated minute tubercles
confluent caseous foci
or large areas of caseation necrosis (advanced fibrocaseous tuberculosis)
In the progress of this disease, the pleura is inevitably involved, and, depending on the chronicity of the disease, serous pleural effusions, frank tuberculous empyema, or massive obliterative fibrous pleuritis may be found.
In the course of extensive fibrocaseous tuberculosis, it is almost inevitable that tubercle bacilli become implanted on the mucosal linings of the air passages to produce endobronchial and endotracheal tuberculosis. These lesions may later become ulcerated and produce irregular, ragged, necrotic, mucosal ulcers. Accompanying the endobronchial tuberculosis, laryngeal seeding and intestinal tuberculosis may occur. Fortunately, these complications of tuberculosis are now uncommon.
Lymphohematogenous dissemination may give rise to miliary tuberculosis, confined only to the lungs or also involving other organs. The distribution of miliary lesions depends on the pathways of dissemination. Tuberculous infection may drain via the lymphatics through the major lymphatic ducts into the right side of the heart and then spread into a diffuse, blood-borne pattern throughout the lungs alone. Despite their small size, most of the bacilli are usually filtered out by the alveolar capillary bed. Therefore, the infective material may not reach the arterial systemic circulation.
Such limitation to the lungs usually is not complete, however, and some bacilli pass through the capillaries or through lymphatic-vascular anastomoses to enter the systemic circulation and produce distant organ seedings. Favored targets for miliary seeding are
the bone marrow
which provide sites for biopsy or direct visualization of disease (retina).
Occasionally, isolated organ involvement is found (e.g., kidneys, adrenals, testes). In the miliary type of distribution, individual lesions vary from one to several millimeters in diameter and are distinct, yellow-white, firm areas of consolidation that usually do not have grossly visible central caseation necrosis or cavitation at the time of examination. Histologically, however, these present the characteristic pattern of individual or multiple confluent tubercles having microscopic central caseation.
In the highly susceptible, highly sensitized individual, the tuberculous infection may spread rapidly throughout large areas of lung parenchyma and produce a diffuse bronchopneumonia, or lobar exudative consolidation, at one time descriptively referred to as galloping consumption.
Sometimes, with such overwhelming disease, well-developed tubercles do not form, and it may be difficult to establish on histologic grounds the tuberculous nature of the pneumonic process. Numerous bacilli, however, are usually present in such exudates.