Is caused by the tubercle bacillus and may be either a local disease or a part of a general involvement. The infection may gain entrance to the lungs in three ways: by the air, aero genie or bronchogenic; by the blood, hematogenic; or by the lymph-channels, lymphogenic. All three methods are finally closely associated.
The tubercle bacilli gain entrance by adhering to dust particles or by "droplet infection".
In this latter the fine spray from sneezing or coughing will contain many bacilli and may be inspired by anyone within a range of several feet. They pass down the bronchi, finally becoming lodged upon the mucous membrane of either the air-vesicles or the terminal bronchioles. The apex of the lung is the portion generally involved at first. The bacilli act upon the mucosa as an irritant and set up a mild catarrhal inflammation. The alveoli become filled with desquamated epithelium and leukocytes. This constitutes the primitive tubercle. In it there is a central zone of degeneration a median zone in which epithelioid, giant and round cells, as well as bacilli, are present, and a peripheral zone which contains many round cells but few epithelioid. The bacilli may grow in the air-cells or may be carried by the leukocytes into the lymphatics, so that the original tubercle may be either alveolar or interstitial, or, if around the bronchi, peribronchial. As the organisms increase in number there is an increase in the extent of the tubercle, thus involving neighboring alveoli. These undergo the same changes as the one originally infected. As this process extends there is destruction of the capillary vessels in the tubercles, and as no new ones are formed, there is a loss of nutrition. As a result there is coagulation necrosis of the central part of the tubercle. While this is taking place there is a proliferation of the fixed connective-tissue cells in the structures surrounding the diseased area; round-cell infiltration also occurs.
The tubercle, as it increases in size, approaches and coalesces with neighboring ones till large areas form. The central portion, showing coagulation necrosis, finally opens into a bronchus, escapes, and leaves a ragged cavity behind. Bloodvessels will be exposed, and if destruction occurs before obstructive endarteritis takes place there will be hemorrhages of varying degrees of severity. The blood that does escape furnishes an excellent culture media for saprophytic bacteria. The bronchus may be evident or its walls may have been completely destroyed.
When communication has been effected between a tuberculous focus and the outside air secondary infection by pyogenic organisms occurs. At the same time the tubercular material is carried along the bronchi during the respiratory acts and other foci are established. The lymphatics carry the bacilli into other parts and there is also involvement of the blood-channels. Consequently all three methods of infection are being made use of and the entire lung may become converted into one mass of broken-down caseous material.
Fig. 144. - Peribronchial Tubercle of the Lung and Caseous Pneumonia of the Adjacent Alveoli (Stengel).
In the bronchogenic form the caseation is particularly marked, while in the hematogenic and lymphogenic the involvement is more distinctly miliary. Of the caseous, three different forms are described: The acute caseous or galloping phthisis; the chronic ulcerative, and the fibrous or fibroid type. This is not an accurate clinical division, as all three processes may be present in the same lung.
Acute caseous tuberculosis, caseous bronchitis, occurs most frequently in children. The process is usually quite rapid in this form and the lung resembles somewhat closely the stage of gray hepatization of croupous pneumonia. The infection is at first lobular, but by extension may involve an entire lobe. Either the base or the apex is the seat of the primary focus.
Fig. 145. - Subacute Caseous (Tuberculous) Pneumonia (Bollinger).
The cut surface of the lung will show irregular yellowish caseous areas with congestion of the intervening pulmonary tissue. On account of the process being acute there is no cavity formation. If cavities are found they are due to a pre-existing, chronic ulcerative tuberculosis. The yellowish areas when closly examined will be seen to consist of bronchi surrounded by caseous material and more or less filled with the cheesy exudate.
The lumen, as a rule, is very rarely obliterated completely. Numerous small excavations form, but there is little attempt at fibrous formation.
If the infection is less severe, there is less confluence of the degenerated areas, and instead of a general infiltration, scattered patches of caseous pneumonia are seen throughout the lung. There is also more fibrous growth, some of the areas becoming completely encapsulated.
Chronic ulcerative tuberculosis is the form most generally met with. It usually begins in the apices and is characterized by the formation of quite extensive cavities. These result from degeneration and necrosis of the lung tissue. Several cavities may coalesce and form a single large one. A large part of the ulcerative process is due to secondary infection by pyogenic organisms. The inner surface of the cavities is rough and irregular, arteries and strands of lung tissue being present. There is fibrous proliferation in the walls, while in the cavity itself there is a secretion containing broken-down caseous material, pus cells, epithelium, and tubercle bacilli and the organisms of the secondary infection.
The arteries traversing the cavities may be the seat of small aneurysms which may rupture and give rise to a fatal hemorrhage. Hemorrhage does not always result when the blood vessels are destroyed as there may have been an obliterating endarteritis resulting from the inflammation.
The healing processes, although well marked in places, are unable, as a rule, to keep pace with the necrosis, and the patient eventually succumbs.
This may occur as an essentially chronic condition or it may follow upon acute processes with cavity formation. Surrounding the caseous areas there is a proliferation of connective tissue with encapsulation and the contained material may become completely infiltrated with lime salts. It may be merely surrounded by a capsule, and if anything should occur that should cause destruction of the enveloping tissue, the caseous material could give rise to acute processes, the activity of the tubercle bacilli not having suffered by their confinement.
The newly formed fibrous tissue is, in a way, of distinct disadvantage, as by its shrinking it causes distortion with diminishment in the size of the lung.
Fig. 146. - Tuberculosis of the Lung (McFarland).
The upper lobe shows advanced cheesy consolidation with cavity-formation, bronchiectasis, and fibroid changes; the lower lobe retains its spongy texture, but contains numerous miliary tubercles.
This form results from the entrance of the infecting material into the blood-stream, and is usually part of a general tuberculosis of the body, but it may be limited to a single lung. The bacilli lodge in the capillaries in the form of emboli and set up minute foci of degeneration - miliary tubercles. These are small grayish areas formed in the same way as tubercles elsewhere. When the lungs are alone involved the condition is called miliary tuberculosis of the lungs.
In this the infection generally results from the bacilli being carried from the lymph-nodes, where they have lodged, into the lung tissue by means of the lymphatics. A tuberculous lymph-node may soften and discharge into a bronchus, a form of secondary aŽrogenous infection. Extension may occur from a tuberculous pleurisy. In such cases there is frequently associated a suppurative lymphangitis. The processes in the lymphogenic form are quite similar to the hematogenic variety and show tubercle formation.
A patient recovers from tuberculosis when the lung becomes sufficiently immunized to resist further progress of the bacilli. In such cases the tubercles will have been encapsulated by new-formed fibrous tissue, isolated and calcified.
Tuberculosis of the lungs may be complicated by secondary infections elsewhere, particularly of the intestines. This results from the swallowing of the infectious sputum and is most common in adults. The larynx may be involved in the same way. There may be infection of the pleura with the formation of adhesions that can interfere very much with respiration. Lobar pneumonia may involve the non-tuberculous areas of the lung or emphysema may be present. Pneumothorax may be caused by the tuberculous process rupturing into the pleural cavity, with collapse of the lung. There is usually an accompanying empyema resulting from the infection of the pleura by the discharged material. Hemorrhage, hemoptysis, is the most dangerous and common complication. It may follow the rupture of a small aneurysm or the erosion of a vessel before a thrombus has had time to form. It may be slight or very severe. Some of the blood may remain within the lung and, forming a good medium for the growth of saprophytic organisms, give rise to gangrene. •
The apices are the most common primary seat. This is probably due to the fact that their bronchi come off at such an angle that they are easily obstructed; that on account of being furthest away from the entrance of the blood-vessels they are more poorly nourished, and that the apex undergoes the least distention during respiration.