Which tuberculosis is the most dangerous? Types, forms and complications. Tuberculosis of unknown localization
Primary tuberculosis- a disease coinciding with the period of primary infection.
Features of primary tuberculosis
Childhood (may occur in HIV-infected or severely weakened patients), pronounced sensitization and the presence of paraspecific reactions (vasculitis, arthritis, serositis); tendency to hematogenous and especially lymphogenous generalization, lymphotropy, the possibility of self-healing during the formation of immunity.
Morphological expression primary tuberculosis - primary tuberculosis complex. It consists of 3 components: primary affect, or focus (focus of lesion in the organ), lymphangitis (tuberculous lesion of the abducens lymphatic vessels) and lymphadenitis (tuberculous inflammation of regional lymph nodes). The primary complex in tuberculosis is a variant of the primary infectious complex.
In case of airborne infection the lung is affected. Primary affect, i.e. the focus of the primary injury is a small tubercle or a larger lesion caseous necrosis, most often located under the pleura in right lung, in well-aerated segments - III, VIII, IX and X. The focus can occupy several alveoli, an acinus, a lobule or even a segment. Characteristic involvement of the pleura is fibrinous or serous-fibrinous pleurisy. Tuberculous lymphangitis manifested by lymphostasis and tuberculous tubercles in the perivascular tissue. Since mycobacterium-infected macrophages enter regional lymph nodes, first in one, and then in many bronchopulmonary, bronchial and bifurcation lymph nodes, granulomatous inflammation with caseous necrosis also develops - lymphadenitis. Changes in the lymph nodes are always more pronounced compared to the primary affect.
In case of nutritional infection The primary tuberculosis complex develops in the intestine. Primary affect in the form of an ulcer is formed in lymphoid tissue the lower part of the jejunum or cecum, lymphadenitis occurs in the regional lymph nodes, and lymphangitis occurs along the lymphatic vessels. A primary tuberculous affect in the tonsil or skin (in the form of an ulcer) with lymphangitis and regional tuberculous lymphadenitis is possible.
There are three variants of the course of primary tuberculosis
1) attenuation of primary tuberculosis and healing of foci of the primary complex;
2) progression of primary tuberculosis with generalization of the process;
3) chronic course (chronically current primary tuberculosis).
Attenuation of primary tuberculosis And healing of lesions of the primary complex starts in a few weeks. T-lymphocyte-mediated immunity develops, which can be determined by the appearance of a positive skin test ( skin test angle). During the formation of anti-tuberculosis immunity, activated macrophages gradually destroy the phagocytosed pathogen, a scar is formed in the zone of primary affect or dehydration, petrification (dystrophic calcification) and encapsulation occur. The wide fibrous capsule may contain foci of fibrous metaplasia connective tissue into the bone ( ossification). The healed primary affect in the lung is called hotbed of Gon. This area may have different sizes, but rarely exceeds 1 cm. It can serve as a receptacle for an inactive pathogen in carriers of infection. Those zones of the primary complex where cheesy necrosis has developed undergo fibrosis and petrification. This is how it is formed Gona complex(petrification at the site of the primary affect, petrification in the lymph node, fibrosis along the course of lymphadenitis). It should be noted that in the lymph nodes healing proceeds more slowly and the pathogen persists longer than in the pulmonary focus. A petrified paratracheal lymph node, a sign of the former primary tuberculosis complex, persists throughout life and can be identified during an X-ray examination of the lungs.
During healing, a scar forms in the intestine at the site of the primary ulcer, and petrification forms in the lymph nodes.
Progression of primary tuberculosis with generalization of the process
manifests itself in following forms: growth of primary affect, hematogenous, lymphogenous, through anatomical channels, mixed.
The growth of primary affect is the most severe form of progression of primary tuberculosis. An increase in the primary affect can lead to lobar caseous pneumonia; when the cheesy masses are removed, an acute cavity is formed - primary pulmonary cavity. If the process takes a chronic course, primary pulmonary consumption develops, resembling secondary fibrous-cavernous tuberculosis. Extensive caseous pneumonia often ends in death from “fleeting consumption.”
Canalicular (through natural anatomical channels) and hematogenous spread (progression) are expressed in 3 forms. 1st form - rapidly developing large focal pulmonary lesions(with caseous necrosis). 2nd form - miliary tuberculosis with generalization of the process and the appearance of millet-like lesions in the lungs and other organs. 3rd form - basilar leptomeningitis(damage to the soft meninges). Very rarely observed acute tuberculous sepsis in combination with meningitis. With hematogenous generalization, foci of elimination are formed, which can subsequently, sometimes many years after the primary infection subsides, become sources of reinfection. They are usually localized in the lungs (small symmetrical petrificates in the apices of the lungs - Simon's hearths), kidneys, genitals and bones.
The lymphogenic form of progression is manifested by the involvement in the process of specific inflammation of the bronchial, bifurcation, paratracheal, supra- and subclavian, cervical and other lymph nodes. Enlargement of the affected cervical lymph nodes, which contributes to thickening of the neck, is called scrofula. Tuberculous bronchoadenitis can be complicated by bronchial obstruction when the contents of a caseous lymph node rupture into the bronchus ( adenobronchial fistulas), compression of the bronchus with the appearance of foci of atelectasis, bronchiectasis.
Chronic course (chronically current primary tuberculosis) is rare these days, mainly among socially unsettled people young(25-35 years old). This form is based on the slow progression of specific inflammation in the lymph nodes, sometimes with the primary affect already healed. More and more groups of lymph nodes are involved, the disease is characterized long course With periodic exacerbations. Skin fistulas with chronic lymphorrhea may form, but this phenomenon is rare. The diagnosis is usually made through surgical biopsy and morphological examination of the lymph node.
Primary tuberculosis
Primary tuberculosis is a process that develops as a result of primary infection of previously uninfected people.
Secondary tuberculosis, which is detected in the vast majority of patients, develops against the background of a previous primary infection or cured primary tuberculosis. The occurrence of secondary tuberculosis is associated with a violation of the body's resistance and may depend on superinfection, i.e. re-infection the body by mycobacteria, as well as from endogenous reactivation of residual tuberculous changes existing in the body. Sometimes both of these factors are important in the pathogenesis of the disease. Conducted genetic research in the pathogenesis of modern tuberculosis, an increased role of exogenous superinfection has been established, which in some cases may be caused by resistant MBT strains.
Primary tuberculosis mainly occurs in children and adolescents. The most significant risk factors for its development are
1. lack of vaccination
2. contact with a patient with tuberculosis
3. pronounced and hyperergic Mantoux reaction, its turn, increase in the size of the papule compared to the previous one, lack of chemoprophylaxis in these cases
4. absence of a scar after BCG vaccination.
Have a certain significance accompanying illnesses, social status, especially in the presence of contact, hereditary predisposition.
The main features of primary tuberculosis are: damage lymphatic system with the accumulation of the pathogen primarily in the lymph nodes, lympho-hematogenous spread of tuberculosis infection, a tendency to high level specific sensitization, frequent involvement in the process serous membranes, primarily the pleura, as well as extrapulmonary localizations. It is possible to develop paraspecific reactions such as erythema nodosum, phlyctenular keratoconjunctivitis, etc. There is a high incidence of tuberculous lesions of the bronchi.
The course of primary tuberculosis is generally benign, the disease tends to heal itself. However, in this case, pronounced residual changes occur, which are the source of secondary tuberculosis. They do not develop when timely detection and treatment.
With regular tuberculin diagnostics, correct assessment of tuberculin reactions, timely appointment chemoprophylaxis, primary tuberculosis develops very rarely. Great importance Vaccination and revaccination with BCG also help prevent it.
There are several forms of primary tuberculosis:
1. tuberculosis intoxication
2. primary tuberculosis complex
3. tuberculosis of intrathoracic lymph nodes
4. chronically current primary tuberculosis.
According to its genesis, primary tuberculosis in some patients may also include tuberculosis of peripheral and mesenteric lymph nodes, miliary, disseminated tuberculosis, tuberculous meningitis, pleurisy and polyserositis. Currently, the structure of clinical forms of primary tuberculosis is dominated by lymphadenitis, mainly of the intrathoracic lymph nodes; primary tuberculosis complex in about 25% of cases, pleurisy in 12–15% of cases. Miliary, disseminated tuberculosis, tuberculous meningitis in children in Belarus are extremely rare. Transition of primary tuberculosis to chronic forms also rare, accompanied by a long wave-like course with damage to the lymph nodes and the development of paraspecific reactions, the so-called “tuberculosis masks”: keratoconjunctivitis and blepharitis, joint damage, known as Poncet’s rheumatism, as well as leukemoid reactions, changes in the cardiovascular and nervous systems. Secondary tuberculosis is characterized by a wide variety of clinical forms and pathomorphological manifestations, especially in the chronic course of the disease with alternating periods of exacerbation and subsidence of the process characteristic of tuberculosis.
Pathogenesis of the early period of primary tuberculosis infection.
Already at the beginning of the last century, data appeared about the possibility of a latent primary tuberculosis infection in the human body without obvious manifestations, both clinical and morphological. A.I. Kagramanov proposed the term “latent microbiism” for a similar situation. This condition can occur with sufficiently high resistance and a small number of mycobacterium tuberculosis entering the body.
Mycobacterium tuberculosis, which has penetrated the body regardless of the route of infection, is capable of rapidly spreading in it by lymphogenous and hematogenously, getting into various organs and tissues, but first of all, settling in the lymphatic system (lymph nodes). Often the state of “latent microbiism” is only initial stages in the interaction of tuberculosis infection and the macroorganism. Tuberculin tests also negative. This period is also called pre-allergic. Its duration is usually in the majority of primary infected patients in various organs and tissues, changes occur that are called paraspecific. They are of toxicoallergic origin, diverse, and characterized by cellular polymorphism. These may be vasculitis, diffuse and nodular macrophage reaction, etc.
Clinical manifestations early tuberculosis infection are individual and depend on the condition protective forces organism, virulence, massiveness of infection and frequency of infection. In most children and adolescents, it is asymptomatic or low-symptomatic, manifesting itself in a turn of the tuberculin reaction, the appearance of which indicates the onset of early period primary infection, as well as increased fatigue, decreased appetite, slight weight loss, pallor skin, the appearance of slight hyperplasia of the cervical and axillary lymph nodes.
Such changes, coinciding in time with the turn of the tuberculin reaction, should be regarded not as tuberculosis disease, but as a primary infection. With chemoprophylaxis, these phenomena quickly disappear.
Complications local forms primary tuberculosis
Complicated course of primary forms of tuberculosis in children and adolescents occurs when the disease is detected late; in those living in foci of tuberculosis (family, related contacts, double, triple contacts with tuberculosis patients) - in case of untimely detection and lack of necessary preventive work among children and adolescents; in children early age from foci of tuberculosis.
Structure of complications from local forms of primary tuberculosis in children and adolescents:
1) bronchial tuberculosis;
2) atelectasis;
3) bronchopulmonary lesions;
4) hematogenous, lymphogenous, less often – bronchogenic dissemination;
5) pleurisy;
6) primary cavity;
7) caseous pneumonia.
Complications of primary forms of tuberculosis occur mainly in patients identified by referral (these are young children and adolescents), as well as by the epidemic method, i.e., by tuberculosis contact.
Bronchial tuberculosis
This is the most common complication and develops as a result of the spread of infection from the primary focus in the lung or intrathoracic lymph nodes. Available contact path lesions (transition of infection from the affected lymph node to the bronchial wall). Specific changes in the bronchi are diagnosed in 17–30% of patients, depending on the timing of detection of the disease. The leading symptom of bronchial tuberculosis is a cough (dry or with sputum production). Diagnosis of this lesion is based on bronchoscopy. There are infiltrative, fistulous (or fistulous) and ulcerative forms of bronchial tuberculosis. Infiltrates have irregular oval shape, unclear boundaries, the mucous membrane often bleeds. The fistulous form is characterized by infiltration of the bronchial wall, to which a caseous-changed node is adjacent, then a whitish area is formed in the center of the infiltration, after a breakthrough of which a fistula opening is formed. Ulcerative form is productive, there is a proliferation of granulations around the fistula tract. The outcome of bronchial tuberculosis is stenosis due to cicatricial changes in the bronchus. Stenosis can be I, II or III degree. There may be deformation of the bronchial wall. At late diagnosis tuberculosis in children and adolescents, it is possible to identify the outcomes of bronchial tuberculosis: limited scar changes, confirming the complicated course of primary tuberculosis.
Atelectasis
Impaired bronchial obstruction leads to the development of atelectasis of the lung tissue. Radiologically, this appears as a uniform darkening with a decrease in the volume of the affected area. The area of atelectasis can occupy a segment, several segments, or an entire lobe. The contours of atelectasis are clear. Adjacent sections are hyperaerated, adjacent organs are shifted towards atelectasis.
Bronchopulmonary lesions
In the pathogenesis of lobar and segmental processes, a significant role is played by specific damage to the intrathoracic lymph nodes, as well as the subsequent development of bronchial tuberculosis.
Lung tissue can contain a variety of morphological changes which are associated with impaired bronchial obstruction - atelectasis; with the spread of MBT by the bronchogenic route (foci of specific inflammation); with the addition of nonspecific flora (foci nonspecific inflammation). Clinical signs with bronchopulmonary lesions are expressed in varying degrees and depend on the age of the child, the timing of the development of complications. During atelectatic-pneumonic processes in the lung tissue, foci of specific and nonspecific inflammation are determined along with atelectatic changes.
Outcomes depend on the timing of complications and the adequacy of therapy. If treatment is started during the period of atelectatic and atelectatic-pneumonic changes, then it is possible favorable outcome. When a complication is detected late, pneumosclerosis develops with foci of calcification.
Hematogenous and lymphogenous dissemination
Hematogenous and lymphogenous dissemination in limited or generalized volumes occurs most often in children or adolescents living in foci of tuberculosis, especially with late diagnosis of the disease and untimely establishment of family contact. Limited dissemination is manifested due to lymphohematogenous spread of MBT from primary foci (PTK, TVGLU) and is usually localized in the upper parts of the lung. Dissemination to other organs leads to the development of extrapulmonary forms of tuberculosis.
Generalized dissemination of MTB most often develops during fresh primary processes, mainly in young children from foci of tuberculosis. The most severe forms of this dissemination are miliary tuberculosis, tuberculous sepsis, and tuberculosis of the central nervous system.
Example. A 2-year-old boy from a family contact of MBT+ tuberculosis. The child’s disease was identified during a contact examination. Frequent ARVI for the last 8 months. BCG - at birth. Symptoms of intoxication are clear: decreased appetite, lethargic, body weight - 10.5 kg, peripheral lymph nodes in VII groups small, elastically compacted. In the lungs on the right in the upper sections there is weakened breathing, heart sounds are muffled, the liver protrudes from under the edge of the costal arch by 2.0 cm. In the blood test: Hb - 92 g/l, l = 8.5? 109, neutrophils – 48%, lymphocytes – 39, monocytes – 12, eosinophils – 4%, ESR – 28 mm/h.
X-ray: expansion of the mediastinum to the right due to an increase in intrathoracic lymph nodes of the paratracheal, bronchopulmonary and bifurcation groups, dropout foci in upper lobe right lung.
Pleurisy
Pleurisy in children and adolescents can be both complications of primary forms and an independent form of the disease. They are discussed in detail in a special section of this reference book.
Primary cavity
If the primary tuberculosis complex is not diagnosed in a timely manner in children and adolescents from foci of tuberculosis infection, the disease may progress and a decay cavity may form in the area of primary affect. IN last years This form of PTC has become more common in young children. Clinical signs of the disease with the development of a decay cavity are clearly expressed: loss of appetite, low-grade fever body, cough with sputum, sometimes hemoptysis. In the lung they are heard hard breathing and loud wheezing. In the blood – neutrophilic shift to the left, lymphopenia, ESR – 25–45 mm/h. The Mantoux reaction with 2TE is normergic or hyperergic. X-ray in the upper or middle sections in the zone of primary affect, located subpleurally, shows a site of destruction. Small or large foci of screening are usually located around the lesion.
Initially, the decay zone is vaguely limited from the surrounding infiltrative tissue, the contours of the cavity from the inside are uneven due to the presence of necrotic masses that have not yet melted. Gradually the cavity is cleared - and it internal walls become smooth. Rarely is the liquid level in the cavity determined. Sometimes decay begins in several places and multiple small cavities appear. With progression, the decay cavity can become a source of bronchogenic contamination. Complete treatment leads to closure of the cavity and the formation of a lesion or pneumosclerosis. In cases of late diagnosis, a combination of complications such as decay and contamination, bronchogenic damage against the background of a significant increase in VGLU is observed.
Caseous pneumonia
Caseous pneumonia is now rare, mainly in children in the first 5 years of life. But its prognosis is difficult, especially in young children.
Caseous pneumonia is the result of progression of PTC and usually has the character of lobar or segmental pneumonia.
Expansion noted lung root, emphysema of pulmonary tissue against the background of pronounced infiltrative changes with areas of caseous necrosis. In young children, infiltration takes a large extent, decay occurs intensively, the size of the cavities increases, dissemination and the development of pleurisy are more often observed. Clinical picture: severe intoxication, chills, sudden heavy sweats, fever of the wrong type. Objectively: loss of body weight, shortening of percussion sound, multiple moist rales of various sizes, areas of weakened and bronchial breathing. Hemogram: hypochromic anemia, leukocytosis, band shift, lymphopenia, monocytosis, ESR up to 50–60 mm/h. Caseous pneumonia requires intensive tuberculostatic, pathogenetic therapy. Outcomes of caseous pneumonia: area of fibrosis, cirrhosis, transition to fibrous-cavernous tuberculosis.
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Tuberculosis intoxication is an early clinical form of primary tuberculosis with minimal specific damage. It develops in people with relatively small functional disorders V immune system. As a result of the formation of toxic products, transient bacteremia and toxemia occur, increasing the specific sensitization of tissues to mycobacteria and their metabolic products and increasing the tendency to severe toxic-allergic tissue reactions.
Mycobacteria during tuberculosis intoxication are mainly found in the lymphatic system, gradually settling in the lymph nodes and causing hyperplasia of lymphoid tissue. As a result, micropolyadenopathy develops, characteristic of all forms of primary tuberculosis.
Tuberculosis intoxication manifests itself in various functional disorders, high sensitivity to tuberculin and micropolyadenopathy. The duration of tuberculosis intoxication as a form of primary tuberculosis does not exceed 8 months. It usually proceeds favorably. The specific inflammatory reaction gradually subsides, single tuberculous granulomas undergo connective tissue transformation. In the area of tuberculous necrosis, calcium salts are deposited and microcalcifications are formed.
Sometimes tuberculosis intoxication becomes chronic or progresses with the formation of local forms of primary tuberculosis. The reverse development of tuberculosis intoxication is accelerated by treatment with anti-tuberculosis drugs.
Tuberculosis of the intrathoracic lymph nodes
Tuberculosis of the hilar lymph nodes is the most common clinical form of primary tuberculosis, affecting various groups of hilar lymph nodes. Inflammation most often develops in the lymph nodes of the bronchopulmonary and tracheobronchial groups, usually without involvement specific process lung tissue. Tuberculous lesions of the lymph nodes of the bronchopulmonary group are often called bronchoadenitis.
After infection with Mycobacterium tuberculosis, a hyperplastic reaction develops in the lymph nodes, followed by the formation of tuberculous granulomas. The progression of specific inflammation leads to the gradual replacement of lymphoid tissue with tuberculous granulations. The area of caseous necrosis can increase significantly over time and spread to almost the entire lymph node. Paraspecific and nonspecific inflammatory changes occur in the tissue adjacent to the lymph node, bronchi, vessels, nerve trunks, and mediastinal pleura. The pathological process progresses and invades other, previously unchanged mediastinal lymph nodes. The total volume of local damage can be quite significant.
Depending on the size of the affected intrathoracic lymph nodes and the nature of the inflammatory process, infiltrative and tumorous (tumor-like) forms of the disease are conventionally distinguished. The infiltrative form is understood as a predominantly hyperplastic reaction of the lymph node tissue with minor caseous necrosis and perifocal infiltration. The tumorous form is associated with pronounced caseous necrosis in the lymph node and a very weak infiltrative reaction in the surrounding tissues.
The course of uncomplicated tuberculosis of the intrathoracic lymph nodes is often favorable, especially with early diagnosis and timely treatment. Perifocal infiltration resolves, calcifications form in place of caseous masses, the lymph node capsule hyalinizes, and fibrous changes develop. Clinical cure with the formation of characteristic residual changes occurs on average 2-3 years from the onset of the disease.
Complicated or progressive course of tuberculosis of the intrathoracic lymph nodes can lead to specific damage to the lung 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, affecting as the primary tuberculosis complex is associated with high virulence of the pathogen and significant impairment of cellular immunity.
Primary tuberculosis complex is a local clinical form of primary tuberculosis, in which three components of a specific lesion are distinguished: primary affect with a perifocal reaction, tuberculosis of the regional lymph node and the connecting zone of tuberculous lymphangitis.
Primary tuberculosis complex with damage to the lung and intrathoracic lymph nodes can develop in two ways. With massive airborne infection With virulent Mycobacterium tuberculosis at the site of their penetration into the lung tissue, a primary pulmonary affect occurs in the form of acinous or lobular caseous pneumonia with a zone of perifocal inflammation. The affect is localized in well-ventilated parts of the lung, usually subpleural. The inflammatory reaction spreads to the walls of the lymphatic vessels. Mycobacterium tuberculosis penetrates the regional lymph nodes through the lymph flow. The introduction of mycobacteria leads to hyperplasia of lymphoid tissue and the development of inflammation, which after a short-term nonspecific exudative phase acquires a specific character.
This is how a complex is formed, consisting of the affected area of the lung, specific lymphangitis and a zone of tuberculous inflammation in the regional lymph nodes.
In addition, during aerogenic infection, Mycobacterium tuberculosis can penetrate through the intact bronchial mucosa into the peribronchial lymphatic plexuses and. further, to the lymph nodes of the root of the lung and mediastinum, where specific inflammation develops. A nonspecific inflammatory reaction occurs in the adjacent tissues. The resulting disorders lead to lymphostasis and dilation of lymphatic vessels.
A lymphogenous retrograde path of development is possible. When inflammation spreads from the lymph node to the wall of the adjacent bronchus, mycobacteria can penetrate into the lung tissue through the bronchogenic route. The introduction of mycobacteria into the lung tissue causes the development inflammatory reaction, which usually involves the terminal bronchiole, several acini and lobules. Inflammation quickly acquires a specific character: a zone of caseous necrosis is formed, surrounded by granulations. Thus, following damage to the intrathoracic lymph nodes, the pulmonary component of the primary tuberculosis complex is formed.
In the primary tuberculosis complex, widespread specific, pronounced paraspecific and nonspecific changes are observed. Nevertheless, the tendency towards a benign course of the disease remains. The reverse development occurs slowly. Positive result contribute early diagnosis primary tuberculosis complex and timely initiation of adequate treatment.
With the reverse development of the primary tuberculosis complex, perifocal infiltration gradually resolves, granulations transform into fibrous tissue, caseous masses become compacted and impregnated with calcium salts. A hyaline capsule develops around the emerging lesion. Gradually, a Gohn's focus forms in place of the pulmonary component. Over time, Gon's lesion may undergo ossification. In the lymph nodes, similar reparative processes occur somewhat more slowly and also culminate in the formation of calcifications. Treatment of lymphangitis is accompanied by fibrous compaction of the peribronchial and perivascular tissues.
The formation of a Ghon lesion in the lung tissue and the formation of calcifications in the lymph nodes is 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, wavy, steadily progressing course. In the lymph nodes, along with slowly forming calcifications, fresh caseous-necrotic changes are detected. IN pathological process New groups of lymph nodes are gradually involved, repeated waves of lymphohematogenous dissemination are observed with damage to previously unchanged parts of the lungs. Foci of hematogenous screenings also form in other organs: kidneys, bones, spleen.
For all forms of primary tuberculosis reverse development tuberculosis process And clinical cure are accompanied by the death of most of the mycobacteria and their elimination from the body. However, some mycobacteria are transformed into L-forms and persist in residual post-tuberculosis foci. Modified and incapable of reproducing mycobacteria support non-sterile anti-tuberculosis immunity, which ensures a person’s relative resistance to exogenous tuberculosis infection.
Primary tuberculosis
Primary tuberculosis includes those clinical forms that arise during the period of primary infection and are characterized by unique clinical, radiological and immunobiological signs. They develop, as a rule, during the first year of infection with MBT, with an emphasis on the first 2–6 months. The shorter incubation period(4 weeks), the worse the prognosis. Character traits primary tuberculosis are as follows: 1) primary infection often occurs with high sensitization of all organs and tissues by the waste products of the office, which is accompanied during the “turn” of the tuberculin reaction by pronounced tests (75% of infected people have a Mantoux reaction with 2TE 11 mm or more, up to hyperergic reactions); 2) a tendency to generalize infection predominantly by lymphohematogenous route; 3) lymphotropism, i.e. damage to the lymphatic system: lymph nodes and lymphatic vessels; 4) development of paraspecific reactions: blepharitis, kerato-conjunctivitis, erythema nodosum, arthralgia, etc.; 5) tendency to self-healing; clinical recovery is observed frequently.
The structure of primary tuberculosis is dominated by clinical forms in which damage to the lymph nodes is the main one (tuberculosis of the intrathoracic lymph nodes, tuberculosis of the peripheral lymph nodes).
Damage to the lymph nodes is the main morphological and clinical expression of primary tuberculosis, including chronic tuberculosis. It defines clinical picture, frequency and nature of complications, time and stability of cure.
MBT enter the human body from the environment in most cases through the respiratory tract. The very mechanism of development pulmonary process can be hematogenous, since the perceived infection is not immediately fixed by the lungs and the latter are affected sequentially (after 3–4 weeks or more) when the office circulates in circulatory system. Lung damage is a consequence of specific tuberculous changes in the lymph nodes. Pulmonary infiltration in the classic primary complex is largely due to atelectatic changes due to the transition of the process from enlarged bronchial lymph nodes to the lobar and segmental bronchi. According to Russian pathomorphologists and bronchologists, changes in the bronchi, including segmental and subsegmental, were detected in 25–94% of children with primary tuberculosis complex. Changes in the bronchi more often occurred after 4–12 months. after the development of local forms of tuberculosis.
The dominant moment in the occurrence of clinical forms of primary tuberculosis is the circulation of MTB through the lymphatic system with the subsequent development, mainly in the lymph nodes, of paraspecific and specific changes. The release of MBT beyond the lymphatic system marks the emergence of multiple localizations, mainly hematogenously, in various organs and systems (liver, spleen, intestines, musculoskeletal system, organs of vision, central nervous system and etc.). Tuberculosis of the primary period: this is a non-local form of tuberculosis - tuberculosis intoxication; primary tuberculosis complex; tuberculosis of intrathoracic lymph nodes. In addition, in children, mainly infancy, young children living in the source of infection develop miliary tuberculosis of primary origin. If this severe form of a generalized process is diagnosed late, the child dies.
In a child or adolescent infected with MTB, or after they have suffered from clinical forms of primary tuberculosis, relative immunity to tuberculosis is formed within 1–4 years.
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