Primary tuberculosis: pathogenesis

Primary tuberculosis is accompanied by the defeat of lymph nodes, lungs, pleura, and sometimes in other organs: kidneys, joints, bones, peritoneum. The zone of a specific inflammation can be very small and remain hidden during the examination. With a large amount of damage, it is usually found during clinical and radiation examinations of the patient.

There are three main forms of primary tuberculosis:

• tuberculous intoxication;
• tuberculosis of the intrathoracic lymph nodes;
• primary tuberculosis complex.

[1], [2], [3], [4]

Tuberculosis intoxication

Tuberculosis intoxication is an early clinical form of primary tuberculosis with minimal specific lesion. It develops in people with relatively small functional impairments in the immune system. As a result of the formation of toxic products, transient bacteremia and toxemia occur, which intensify specific sensitization of tissues to mycobacteria and their life products, and increase the tendency to severe toxic-allergic tissue reactions.

Mycobacteria with tuberculous intoxication are mostly in the lymphatic system, gradually settling in the lymph nodes and causing hyperplasia of the lymphoid tissue. As a result, micro-polyadenopathy, which is characteristic of all forms of primary tuberculosis, develops.

Tuberculosis intoxication is manifested by various functional disorders, high sensitivity to tuberculin and micro-polyadenopathy. The duration of tuberculosis intoxication as a form of primary tuberculosis does not exceed 8 months. It flows more often favorably. Specific inflammatory reaction gradually subsides, single tubercular granulomas are subjected to connective tissue transformation. Calcium salt is deposited in the zone of tuberculous necrosis and microcalcinates are formed.

Sometimes tuberculosis intoxication acquires a chronic course or progresses with the formation of local forms of primary tuberculosis. The reverse development of tuberculosis intoxication is accelerated by the treatment with anti-tuberculosis drugs.

Tuberculosis of the intrathoracic lymph nodes

Tuberculosis of the intrathoracic lymph nodes is the most frequent clinical form of primary tuberculosis, affecting various groups of intrathoracic lymph nodes. Inflammation often develops in the lymph nodes of the bronchopulmonary and tracheobronchial groups, usually without involvement in a specific process of lung tissue. Tuberculous lesions of the lymph nodes of the bronchopulmonary group are often called bronchoadenitis.

After infection with mycobacteria tuberculosis in the lymph nodes develops a hyperplastic reaction with the subsequent formation of tubercle granules. Progression of specific inflammation leads to a gradual replacement of lymphoid tissue with tubercular granulations. The zone of caseous necrosis may increase with time and spread almost to the entire lymph node. Paraspecific and nonspecific inflammatory changes occur in the cellular tissue, bronchi, vessels, nerve trunks, mediastinal pleura adjacent to the lymph node. The pathological process progresses and seizes other, previously unchanged lymph nodes of the mediastinum. The total volume of local damage is very significant.

Depending on the size of the affected intrathoracic lymph nodes and the nature of the inflammatory process, the infiltrative and tumorous (tumor-like) forms of the disease are conventionally isolated . Under the infiltrative form is understood mainly hyperplastic reaction of the tissue of the lymph node with insignificant caseous necrosis and perifocal infiltration. Tumorous form is associated with severe caseous necrosis in the lymph node and a very weak infiltration reaction in the surrounding tissues.

The course of uncomplicated tuberculosis of intrathoracic lymph nodes is more often favorable, especially with early diagnosis and timely treatment. Perifocal infiltration resolves, in place of caseous masses calcites are formed, the capsule of the lymph node is hyalineized, and fibrotic changes develop. Clinical cure with the formation of characteristic residual changes occurs on average in 2-3 years from the onset of the disease.

Complicated or progressive course of tuberculosis of the intrathoracic lymph nodes can lead to a specific lesion of the pulmonary tissue. Lymphohematogenous and bronchogenic generalization of the process is observed in patients with progressive disorders in the immune system, which deepen against the background of tuberculosis. More often this occurs with late detection of the disease and inadequate treatment.

Primary tuberculosis complex

Primary tuberculosis complex is the most severe form of primary tuberculosis, it affects how the primary tuberculosis complex is associated with high virulence of the pathogen and significant disorders of cellular immunity.

The primary tuberculosis complex is a local clinical form of primary tuberculosis, in which three components of a specific lesion are identified: primary affect with perifocal reaction, tuberculosis of the regional lymph node and the ligamentous tuberculosis lymphangitis connecting them.

The primary tuberculosis complex with the lesion of the lung and intrathoracic lymph nodes can develop in two ways. When massive aerogenic infection with virulent mycobacteria tuberculosis at the site of their introduction into the pulmonary tissue, primary pulmonary affect occurs in the form of acinous or lobular caseous pneumonia with a zone of perifocal inflammation. Affect is localized in well ventilated parts of the lung, usually subpleural. Inflammatory reaction extends to the walls of lymphatic vessels. Mycobacterium tuberculosis with lymph flow penetrates into the regional lymph nodes. The introduction of mycobacteria leads to hyperplasia of the lymphoid tissue and the development of inflammation, which after a short-term nonspecific exudative phase acquires a specific character.

So a complex is formed, consisting of the affected area of the lung, specific lymphangitis and the zone of tuberculous inflammation in the regional lymph nodes.

In addition, with aerogenic infection, mycobacterium tuberculosis can penetrate through the intact mucosa of the bronchus into the peribronchial lymphatic plexus and. Further, into the lymph nodes of the root of the lung and mediastinum, where a specific inflammation develops. In the tissues adjacent to them, a nonspecific inflammatory reaction occurs. The resulting disorders lead to lymphostasis and lymphatic dilatation.

A lymphogenous retrograde pathway is possible. With the spread of inflammation from the lymph node to the wall of the adjacent bronchus, mycobacteria can penetrate into the lung tissue and bronchogenic way. The introduction of mycobacteria into the lung tissue causes the development of an inflammatory reaction, which usually seizes the terminal bronchioles, several acini and lobules. Inflammation quickly acquires a specific character: a zone of caseous necrosis is formed, surrounded by granulations. So after the defeat of the intrathoracic lymph nodes, a pulmonary component of the primary tuberculosis complex is formed.

In the primary tuberculosis complex, there are widespread specific, pronounced paraspecific and nonspecific changes. Nevertheless, the tendency towards a benign course of the disease persists. Reverse development is slow. A positive result is facilitated by early diagnosis of the primary tuberculosis complex and timely initiated adequate treatment.

With the reverse development of the primary tuberculosis complex, perifocal infiltration is gradually dissipated, the granulations are transformed into fibrous tissue, the caseous masses are densified and saturated with calcium salts. A hyaline capsule develops around the emerging foci. Gradually, on the place of the pulmonary component, the focus of the Gon is formed. Over time, the focus of the Gon may be subjected to ossification. In lymph nodes, similar reparative processes occur somewhat more slowly and also result in the formation of calcinates. Treatment of lymphangitis is accompanied by fibrotic densification of peribronchial and perivascular tissues.

The formation of the Gona focus in the lung tissue and the formation of calcifications in the lymph nodes is a morphological confirmation of the clinical cure of the primary tuberculosis complex, which occurs on average 3.5-5 years after the onset of the disease.

In patients with severe immunodeficiency, primary tuberculosis sometimes acquires a chronic, undulating, steadily progressing course. In the lymph nodes, along with slowly formed calcifications, fresh caseo-necrotic changes are found. In the pathological process, new groups of lymph nodes are gradually involved, repeated waves of lymphohematogenous dissemination with lesions of previously unchanged lungs are noted. Foci of hematogenic screenings are formed in other organs: kidneys, bones, spleen.

With all forms of primary tuberculosis, the reverse development of the tuberculosis process and clinical cure are accompanied by the death of most of the mycobacteria and their elimination from the body. However, some of the mycobacteria are transformed into L-forms and persist in residual post-tuberculosis foci. Changed and incapable of reproduction, mycobacteria maintain non-sterile anti-tuberculosis immunity, which provides relative human resistance to exogenous tuberculosis infection.