What causes infiltrative pulmonary tuberculosis?
The development of infiltrative tuberculosis is associated with the progression of focal tuberculosis, the appearance and rapid expansion of the infiltration zone around fresh or old tuberculosis foci. The spread of perifocal inflammation leads to a significant increase in the volume of damage to the lung tissue. A tuberculous infiltrate is a complex of fresh or old foci with an extensive area of perifocal inflammation. Infiltrates are more often localized in the 1-, 2-, and 6-m segments of the lung, i.e. In those departments where tuberculosis foci are usually located.
In terms of localization and volume of lung tissue damage, bronchopulmonary excretion, usually 2-3 pulmonary lobules, segmental (within one segment), as well as polysegmental or lobar infiltrates, are isolated. Infiltrate, which develops along the course of the main or additional interlobar fissure, is called periscisuritis.
A massive tubercular superinfection, accompanying diseases (diabetes mellitus, alcoholism, drug addiction, HIV infection) contribute to the intensification of the inflammatory reaction around the foci . These factors create the prerequisites for rapid growth in the number of microbial populations. Around the tuberculosis foci an inflammatory reaction develops with a pronounced exudative component. Specific inflammation extends beyond the pulmonary lobe, the total volume of lesions increases. So the bronchial fibroblast infiltrate is formed.
With relatively moderate disturbances of immunological reactivity, the intensity of exudation is relatively small, the cellular infiltration is moderately expressed. The alveoli are filled with macrophages, epithelioid and plasma cells and a relatively small amount of exudate. Inflammatory changes have a mixed exudative-proliferative character and spread relatively slowly. The area of tubercular inflammation is usually limited to the limits of the segment, in it an infiltrate is formed, which is commonly called round.
A significant weakening of local and general immunity contributes to higher rates of growth in the number of microbial populations. Hyperergic reaction of the lung tissue to a large population of virulent and rapidly multiplying mycobacteria causes pronounced exudation. Perifocal inflammation is characterized by the poverty of the cellular composition and the weakly expressed signs of specific inflammation. The alveoli are filled with a tissue fluid containing mainly neutrophils and a small number of macrophages. Expressed a tendency to progression of tuberculosis with rapid damage to many segments of the lung (cloud-like infiltrate). Further progression of immunological disorders is characterized by an increase in T suppressor activity and inhibition of HRT. Macrophage cells die, forming a zone of caseous necrosis. Caseous masses gradually melted and released into the drainage bronchus. So in the zone of progressive tubercular inflammation there is a site of destruction, limited by an inflamed-altered pulmonary tissue. Gradually formed cavity decay, which serves as a source of further bronchogenic and lymphogenous distribution of mycobacteria. Involvement in the pathological process of almost the entire lobe of the lung and the formation of multiple cavities of decay in the affected lobe testify to the formation of the lobite.
Over time, the differences between different infiltrates are largely lost. With a progressing course, infiltrative pulmonary tuberculosis is transformed into caseous pneumonia or cavernous tuberculosis.
The rate of regression of infiltrative tuberculosis depends on the nature of the exudate, the prevalence of the lesion, the extent of caseous necrosis, the reactivity of the patient's body. Infiltrates of small length with serous exudate against the background of adequate treatment can resolve relatively quickly. With serous-fibrinous or hemorrhagic exudate, resorption occurs more slowly and is combined with the development of fibrosis. Caseous masses as the resorption of infiltrative changes are condensed and drained. At the site of the decay cavity, a fibrous focus with inclusions of caseosis is formed. In the future, a linear or stellate scar can form on the site of the focus.