Disseminated pulmonary tuberculosis - What's going on?

Disseminated pulmonary tuberculosis may develop in complicated primary tuberculosis as a result of increased inflammatory response and early generalization of the process. Most often, disseminated tuberculosis occurs several years after clinical cure of primary tuberculosis and formation of residual post-tuberculous changes: Ghon's focus and/or calcification. In these cases, the development of disseminated tuberculosis is associated with late generalization of the tuberculous process.

The main source of mycobacteria spread during the development of disseminated tuberculosis is considered to be residual foci of infection in the intrathoracic lymph nodes, formed during the process of reverse development of the primary period of tuberculosis infection. Sometimes the source of mycobacteria dissemination in the form of a calcified primary focus can be localized in the lung or another organ.

The pathogen can spread throughout the body in various ways, but most often dissemination occurs with the bloodstream. The hematogenous route is the basis for about 90% of all disseminated lesions in tuberculosis.

The likelihood of developing disseminated pulmonary tuberculosis increases with exposure to factors that weaken the human immune system, and with prolonged and close contact with bacteria carriers.

Depending on the route of spread of mycobacteria and the location of tuberculosis foci along the blood and/or lymphatic vessels, disseminated pulmonary tuberculosis can be hematogenous, lymphohematogenous and lymphogenous.

Bacteremia is considered a prerequisite for the development of hematogenous disseminated tuberculosis. However, increased sensitivity of cells and tissues to mycobacteria and changes in the functional state of the nervous and vascular systems are also important for the development of the disease. Violation of cortico-visceral regulation leads to vegetative-vascular dystonia and microcirculation disorders. Blood flow in small vessels slows down, and the pathogen penetrates through the vascular wall into the adjacent tissue. Increased sensitivity of cells to mycobacteria, formed in the primary period of tuberculosis infection, ensures rapid absorption of mycobacteria by macrophages, which then lose their ability to move and settle in the perivascular tissue. Further movement of the pathogen is suspended, but the destruction of mycobacteria is difficult and even impossible due to a decrease in the bactericidal potential of macrophages. As a result, multiple tuberculosis foci are formed in the interstitial tissue of the lungs along the vascular-bronchial bundles. With hematogenous spread of mycobacteria, foci are found in both lungs relatively symmetrically.

Lymphogenous dissemination in the lungs occurs when mycobacteria spread with retrograde lymph flow. The process is caused by the reactivation of inflammation in the intrathoracic lymph nodes and the development of lymphostasis. Lymphogenous dissemination of mycobacteria often leads to unilateral dissemination and predominantly root localization of foci. Bilateral lymphogenous dissemination is also possible. It differs from hematogenous by the asymmetrical location of foci in the lungs.

The nature of the inflammatory reaction and the prevalence of foci in disseminated tuberculosis are determined by the individual reactivity of the organism, the massiveness of bacteremia and the severity of immunological and functional disorders. The size of the foci largely depends on the caliber of the vessels involved in the pathological process.

According to pathomorphological studies, there are three variants of disseminated pulmonary tuberculosis. They correspond to the clinical features of its course: acute, subacute and chronic.

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Acute disseminated pulmonary tuberculosis

Acute disseminated pulmonary tuberculosis occurs with a significant decrease in anti-tuberculosis immunity and massive bacteremia. The hyperergic reaction of the pulmonary capillaries to bacterial aggression with a significant increase in the permeability of their walls creates favorable conditions for the penetration of mycobacteria into the alveolar septa and alveolar walls. Along the capillaries, multiple uniform millet-like (from the Latin "milium" - millet), yellowish-gray foci appear almost simultaneously. They protrude above the surface of the lung section in the form of tubercles with a diameter of 1-2 mm and are localized evenly in both lungs. Edema and cellular infiltration of the interalveolar septa significantly reduce the elasticity of the lung tissue. The exudative or caseous-necrotic reaction is very quickly replaced by a productive one, so the foci do not merge. This form of acute disseminated tuberculosis is called miliary.

Sometimes generalization of the tuberculosis process is observed: multiple caseous foci with a large number of mycobacteria are found in other organs (tuberculous sepsis).

With timely diagnosis and full treatment, miliary foci can almost completely resolve. At the same time, signs of emphysema disappear and the elasticity of the lung tissue is restored.

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Subacute disseminated pulmonary tuberculosis

Subacute disseminated pulmonary tuberculosis develops with less severe immune disorders and less massive bacteremia. Intralobular veins and interlobular branches of the pulmonary artery may be involved in the pathological process. The foci formed around the venules and arterioles are medium and large in size (5-10 mm), often merge, forming conglomerates in which destruction may occur. The inflammatory reaction in the foci gradually becomes productive. Productive obliterating vasculitis and lymphangitis develop in the walls of the alveoli and interalveolar septa, and signs of emphysema appear in the lung tissue around the foci.

In subacute disseminated tuberculosis, strict symmetry of lung lesions is not observed. Foci are most often found in the upper and middle sections, mainly subpleurally. Dissemination is not limited to the lungs and often extends to the visceral pleura. The upper respiratory tract, especially the outer ring of the larynx, is often involved in the process.

Specific therapy promotes resorption and compaction of foci. Complete resorption of foci is rarely observed. Fibrous and atrophic changes occur in the interalveolar septa. Emphysema formed in the initial period of the disease becomes irreversible.

Chronic disseminated pulmonary tuberculosis

Chronic disseminated pulmonary tuberculosis usually develops slowly as a result of repeated waves of lymphohematogenous dissemination that are not diagnosed in a timely manner. During the next wave of dissemination, fresh foci appear in intact areas of the lung - where the blood flow was not impaired at the onset of the disease. Repeated waves of dissemination determine the "floor-by-floor" arrangement of foci in both lungs. At first, foci can be found in the apical and posterior segments. The greatest number of foci are found in the upper and middle sections of the lungs. They are localized mainly subpleurally. On the surface of the lung section, a thin looped network of whitish-gray fibrous strands associated with diffuse perivascular and peribronchial fibrosis is clearly visible. Sometimes massive scars in the lung tissue and pleural fibrosis can be found, which indicate a significant age of the tuberculosis process. Fibrous changes are more pronounced in the upper parts of the lungs, and in the lower parts, the development of vicarious emphysema can be observed.

There are significant morphological differences between foci formed at different times. In fresh foci, a pronounced productive tissue reaction predominates. Foci that are very old are surrounded by a capsule. Old foci are partially replaced by fibrous tissue. Sometimes calcium salt inclusions are found in them. Such focal dissemination is called polymorphic.

The tendency for foci to merge and decay to form is weakly expressed, so decay cavities form slowly. They have certain characteristics.

The cavities are usually located in the upper lobes of both lungs, often symmetrically, their lumen is completely free of caseous-necrotic masses; the walls are thin, perifocal infiltration and edema of the surrounding tissues are absent. Such cavities are often called stamped or spectacle caverns.

Significant morphological changes in the lung tissue with a disruption of its biomechanical properties lead to hypertension in the pulmonary circulation, hypertrophy of the right ventricle and the gradual development of pulmonary heart disease.

As a result of repeated waves of hematogenous dissemination by Mycobacterium tuberculosis in patients with chronic disseminated pulmonary tuberculosis, extrapulmonary lesions often form: in the larynx, bones and joints, kidneys, genitals and other organs.

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