Infiltrative Pulmonary Tuberculosis

2024 Author: Josephine Shorter | [email protected]. Last modified: 2023-12-16 21:43

Infiltrative pulmonary tuberculosis

Content:

• Causes of infiltrative pulmonary tuberculosis
• Pathogenesis (what's going on?)
• Symptoms of infiltrative pulmonary tuberculosis
• Diagnosis of infiltrative pulmonary tuberculosis
• Treatment of infiltrative pulmonary tuberculosis
• Prevention of infiltrative pulmonary tuberculosis
• Which doctor should I contact?

One of the forms of focal tuberculosis is infiltrative, which is characterized by an extensive tissue reaction of the lungs. In this phase of the disease, the symptoms of infiltration and focal inflammation come to the fore. There are several reasons that lead to such a development of the pathological process.

In most cases, the mechanism of infiltrative-pneumonic pathogenesis is triggered as a result of an overly violent reaction of the patient's body to the causative agent of tuberculosis, as well as with hypersensitivity of lung tissue in combination with instability of the neuro-vegetative and endocrine systems.

Causes of infiltrative pulmonary tuberculosis

The causative agents of tuberculosis are microorganisms that belong to the type of acid-fast bacteria of the genus Mycobacterium. There are seventy-four types of such mycobacteria known to medicine. They can be found in water, in soil, in humans and animals.

But a person gets sick with tuberculosis only when infected with several types of mycobacteria at once. This disease complex is called M. Tuberculosis and includes the human type Mycobacterium tuberculosis, bovine Mycobacterium bovis, Mycobacterium africanum, Mycobacterium bovis BCG (BCG strain), as well as Mycobacterium canetti and Mycobacterium microti. The group also includes Mycobacterium pinnipedii and Mycobacterium caprae, which from a phylogenetic point of view belong to the type Mycobacterium microti and Mycobacterium bovis.

The main specific feature of mycobacterium tuberculosis (MBT) is their highly pathogenic nature, which is expressed in virulence (infectiousness), which can be modified under the influence of external factors. The manifestations of this virulence depend on the state of the victim's body at the time of the attack of bacteria.

In most cases, a person becomes ill with tuberculosis as a result of infection with bovine and human types of mycobacteria. The maximum number of M. bovis excretions is recorded in rural residents, where the main route of transmission of the pathogen is the alimentary method (through food). Avian tuberculosis occurs mainly in immunocompromised carriers of pathogenic microorganisms.

Mycobacterium tuberculosis belongs to the group of prokaryotes, which are characterized by the absence of highly organized organelles of the Golgi apparatus and lysosomes in the cytoplasm. They also lack the plasmids necessary for genome dynamics, so mycobacterium tuberculosis migrate only with the help of host organisms. These bacteria have a slightly curved or straight configuration, like a rod with rounded ends, one to ten micromicrons long, 0.2-0.6 micron in diameter. Mycobacterium bovine type is thicker and shorter than human.

The microorganisms that cause tuberculosis do not move on their own. They also do not create capsules and microspores.

The cell of such a bacterium consists of:

• Microcapsules, the wall of which is formed by three to four layers, each of which has a thickness of 200-250 nanometers and consists of polysaccharides. The microcapsule is firmly attached to the cell wall and serves as protection from external factors. It has no antigenic properties, but is serologically active;
• The cell wall, which serves as the external boundary of the bacterium, keeps its shape and size stable, protects against mechanical, osmotic and chemical influences and has virulence factors - lipids;
• Homogeneous bacterial cytoplasm;
• Cytoplasmic membrane containing lipoprotein complexes and enzyme systems. It serves to form the intracytoplasmic membrane system (mesosome);
• A nuclear substance containing chromosomes and plasmids.

The antigenic characteristics of MBT are realized in proteins-tuberculoproteins, including tuberculin. They are specific when delayed-type hypersensitivity reactions occur. The presence of polysaccharides in the bacteria helps to detect antibodies in the serum of patients. Lipids give these mycobacteria resistance to acidic and alkaline environments.

Mycobacterium tuberculosis bacteria are aerobic, Mycobacterium bovis and Mycobacterium africanum are aerophilic, meaning they need air to feed and reproduce.

When tuberculosis bacteria damage the lungs, lymph nodes, skin, bones, kidneys, intestines and other organs, a special type of inflammatory process occurs - "cold" inflammation. It is distinguished by a granulomatous character and leads to the appearance of a large number of cavities that are prone to decay.

Pathogenesis of infiltrative pulmonary tuberculosis

As a rule, infection of a primary nature in humans occurs through airborne droplets. Much more rare phenomena are infection through food, household and sexual contact, as well as intrauterine (transplacental) transmission of the pathogen from mother to child.

Bacteria enter the human body when the so-called mucociliary clearance is disturbed, in which the goblet-shaped airway cells create a mucus barrier that traps mycobacteria, and fluctuations in the ciliated epithelium lead to their subsequent evacuation.

The reason for the violation of clearance is usually inflammation in the upper respiratory tract, in the trachea and large bronchi. Toxins also have an effect. As a result, bacteria reach the bronchioles and alveoli, which increases the likelihood of developing the disease.

Due to the fact that mycobacteria do not have the ability to produce exotoxin to stimulate phagocytosis (attack of immune cells), a small number of pathogens do not give rapid manifestations. The structure of the affected tissues remains normal for some time. This is called "latency".

From any point, bacteria with lymph enter the regional lymph nodes, and from there they enter the internal organs with the lymph flow. This process is called primary (or obligate) mycobacteremia.

Pathogens accumulate where the microvasculature is especially developed: in the lungs, in the lymph nodes, in the cortical layer of the kidneys, in the epiphyses and metaphyses of tubular bones, in the fallopian tubes, in the uveal tract of the eyes. The bacteria continue to multiply, but the immune system does not have time to develop.

At this time, in places where most bacteria are collected, phagocytosis begins. Pathogens are attacked and destroyed by polynuclear leukocytes. However, contact with mycobacteria leads to the death of immune cells.

Macrophages, which are involved in the phagocytosis of mycobacteria, are also powerless, since the ATP protons synthesized by MBT, as well as cord factors and sulfates disrupt the functioning of macrophage lysosomes. Being inside macrophages, tuberculosis bacteria grow, divide, and this leads to the death of the host cell. And the office again returns to the intercellular space. It turns out "incomplete phagocytosis".

Acquired cellular immunity

Cellular immunity is formed by macrophages and lymphocytes, effectively interacting with each other. The contact of macrophages, T-helpers and (CD4 +) and T-suppressors (CD8 +) is especially important in this process. Having absorbed mycobacteria, macrophages produce antigens and interleukin-1 (IL-1). It triggers the work of T-lymphocytes (CD4 +). And T-helpers (CD4 +) interact with macrophages and "read" data on the bacterial genome. T-lymphocytes (CD4 + and CD8 +) become sensitized and start producing chemotaxins, gamma interferons and interleukin-2 (IL-2).

This makes the macrophages move faster towards the mycobacteria, and their enzymatic and general bactericidal activity increases. The production of reactive oxygen species and hydrogen peroxide by macrophages is accelerated. An oxygen explosion occurs, which negatively affects the office. L-arginine and tumor necrosis factor-alpha co-induce the formation of nitric oxide NO, which has an antimicrobial effect. The result is a decrease in the destructive effect of MBT on the body and the death of the pathogen.

In a situation where the immune response develops adequately, in each new generation, the immunocompetence of macrophages increases. They produce mediators that activate B-lymphocytes, which are responsible for the synthesis of immunoglobulins. By producing antibodies, leukocytes envelop the MBT, which as a result stick together. And this facilitates phagocytosis.

The growing enzymatic activity of macrophages can provoke the appearance of cells with delayed-type hypersensitivity (PCRT) to antigens of tuberculosis pathogens. As a result, the transformation of macrophages into giant epithelioid cells of Langhans occurs. They are involved in the work to limit the inflamed area.

This leads to the creation of exudative-productive and productive tuberculous granulomas, which is an indicator of a good immune response to the invasion of the MBT and the localization of its aggression.

T- and B-lymphocytes, as well as macrophages in the granuloma, are especially active. There is a transformation of macrophages into epithelioid cells, which are responsible for pinocytosis and the synthesis of hydrolytic enzymes. The central part of the granuloma can be characterized by the appearance of a small area of caseous necrosis, formed from dead macrophages.

The appearance of the PCRT reaction is recorded two to three weeks after the initial infection. The formation of pronounced cellular immunity is observed after eight weeks.

Mycobacteria begin to multiply more slowly, they become smaller, the inflammatory specific reaction subsides. However, the pathogen is not completely destroyed. The remaining bacteria are inside the cells (L-form), which prevents the formation of phagolysosome and makes them inaccessible for the action of lysosomal enzymes. This is a non-sterile form of anti-tuberculosis immunity.

The bacteria that remain in the body preserve the population of sensitized T-lymphocytes and provide immunological activity at a sufficient level. So mycobacteria can exist for a long time, sometimes throughout a person's life. If immunity decreases, mycobacteria can become active and a person can get sick.

A decrease in acquired immunity is provoked by AIDS, diabetes mellitus, and gastric ulcer. May be caused by excessive use of alcohol and drugs. Immunity is negatively affected by fasting, stress, pregnancy, hormone therapy and immunosuppressants. The risk of contracting tuberculosis in a person infected for the first time is eight percent during the first two years, then the likelihood decreases.

The emergence of clinically expressed tuberculosis

If macrophages are not sufficiently activated, phagocytosis has no effect. Mycobacteria multiply very quickly - exponentially. Phagocytic cells die in huge numbers, releasing large volumes of mediators and proteolytic enzymes into the intercellular space. Nearby tissues are damaged, "liquefied". This leads to the formation of a special environment that feeds mycobacteria outside the cells.

The balance of the immune defense is disrupted. T-suppressors (CD8 +) become more, and T-helpers (CD4 +) lose their immunological activity.

PCRT to antigens rises sharply, and then becomes weaker. The inflammation is spreading. The walls of blood vessels become more permeable, plasma proteins penetrate to the tissues along with leukocytes and monocytes. There is a development of tuberculous granulomas with a predominance of caseous necrosis.

Polynuclear leukocytes, macrophages and lymphoid cells infiltrate the outer layer more actively. This leads to the fusion of individual granulomas and an increase in the total volume of the lesion. There is a transition from primary infection to tuberculosis, expressed clinically.

Symptoms of infiltrative pulmonary tuberculosis

Clinical and radiological infiltrates of the following types are possible:

• Bronchobular infiltration is a focus that is located in the cortical sections of the first or second segments of the upper lobe of the lungs, has an irregular rounded shape, the contours are indistinct, the diameter is one to two centimeters. Tomography shows two or three or several fresh, merged foci. Symptoms are not observed, there are no functional changes and bacilli excretion;
• Rounded infiltration means the appearance of foci of darkening, having the shape of a circle or an oval with unsharp contours, the diameter is one and a half to two centimeters. The focus is usually located in the first, second or fourth segment of the lung. From the foci to the root of the lung, an inflammatory "path" runs, against its background a projection of the bronchus is noticeable. X-ray tomography shows denser or calcified foci, small cavities of decay, changes in the pleura, scars. The development of round infiltrates increases the area of perifocal inflammation, leads to the disintegration of the caseous center, and a cavity is formed. It includes sequesters and a little fluid, and is called a pneumonia cavity. Bronchogenic seeding leads to the development of foci of pathogenesis in healthy areas of the lung;
• Cloudy infiltration on X-ray has the form of uneven darkening with blurry contours. Darkening is present in one or more segments in the upper lobes of the lungs. This is similar to nonspecific pneumonia, but the difference is that the radiological changes are persistent, there is a tendency to disintegration and the appearance of cavities;
• Lobitis is an inflammatory process that affects the entire lung lobe. Has a characteristic structure with many caseous foci. The clinical picture is severe. Gradually, the lesion spreads to the entire lobe, on the border of which a clear interlobar groove appears. It has been observed that a small infiltrative focus often develops before the lobitis;
• Periscissuritis, or marginal infiltration, is a cloud-like form that is located near the interlobar sulcus. It is a triangle with the apex turned towards the root of the lung. At the top, the borders are vague, passing into the lung tissue, which is little changed. The border below coincides with the interlobar pleura and has clear contours;
• Caseous pneumonia. A form of the disease that develops in patients with a lack of immunobiological resistance. In the lung tissue, inflammation is observed, where necrosis predominates. Caseous-pneumonic foci extend to the entire lobe or the entire lung.

Various factors provoke caseous pneumonia: power failures, pregnancy, diabetes mellitus, extensive damage to the body by mycobacteria with high virulence. As well as pulmonary bleeding, in which blood is aspirated from the office. Clinically, caseous pneumonia is widespread and has intense morphological changes.

In general, the clinical symptoms of infiltrative tuberculosis are expressed depending on the extent of the lesion. As a rule, the disease begins in an acute form: the patient has a fever, and the symptoms may resemble flu or lobar pneumonia. Manifestations arise against the background of general overall health. Only a thorough survey can reveal signs of tuberculous intoxication, which arose even before the development of acute manifestations.

A common first symptom of this form of the disease is hemoptysis or pulmonary bleeding. The acute period can last for several days or several weeks.

Of the complaints, patients note chest pain on the side where the lung is affected, it is localized in the area of the sides or shoulder blades. There is a dry cough or there is a slight sputum discharge. Signs of intoxication are clearly visible in the form of poor appetite, sweating, sleep disturbances, increased excitability, tachycardia and general weakness.

With caseous pneumonia, the disease begins acutely. The body temperature rises to 40-41 °, there is a big difference between the indicators in the morning and in the evening. Intoxication symptoms worsen rapidly. Adynamia develops sharply, profuse sweat appears, painful sensations in the chest, purulent sputum when coughing, shortness of breath. The person is losing weight quickly.

Diagnosis of infiltrative pulmonary tuberculosis

Physical examination at the onset of the disease reveals a lag in the chest during breathing in the affected side of the lung. The chest muscles are tense, the voice begins to tremble.

Negative data of percussion and auscultation are most pronounced in the case of massive pneumonia of the lobit type, as well as when the infiltration begins to disintegrate and the formation of cavities. On the surface above the affected area, the percussion sound becomes dull, bronchophonia appears, bronchial respiration develops, moist and sonorous persistent rales of various calibers.

Differential diagnosis of infiltrates

With an acute onset of the disease and the rapid development of the pneumonic process in people without tuberculosis in the anamnesis, a diagnosis of "nonspecific pneumonia" is made.

Of particular difficulty is the diagnosis of infiltrative-pneumonic tuberculosis, which is accompanied by influenza syndrome.

Such tuberculosis differs from pneumonia:

• Specific signs of tuberculous intoxication;
• Gradual onset of the disease;
• The absence of catarrhal inflammation in the upper respiratory tract;
• Comparatively satisfactory condition of patients, even at high temperatures.

Nonspecific pneumonia, accompanied by fever, is characterized by a severe condition of patients. At the same time, the specific process (tuberculous) does not have physical manifestations at the onset of the disease: they arise only if the process progresses.

Blood tests of patients show slight shifts in the leukocyte count and a slight increase in ESR. With lobar pneumonia, leukocytosis is high and has a shift to the left, ESR is sharply increased.

X-ray examination shows the localization of tuberculous infiltrates mainly in the upper sections - in the first, second and sixth segments. Inflammatory nonspecific processes are concentrated in the middle and lower fields.

The pictures show a "path" leading from the infiltration to the root of the lung. As a rule, isolated focal shadows are visible at the periphery of the main focus. They can also be observed in other parts of the same or a different lobe of the lung.

Sometimes the diagnosis of tuberculosis can be made only by dynamic observation of the patient and the ineffectiveness of treatment with antibacterial drugs, as well as the presence of mycobacteria in the sputum.

A long period, during which there is a reverse development, is the difference between infiltrative pneumonic tuberculosis and eosinophilic pneumonia: its focus is absorbed quickly, in a few days, and eosinophilia in the blood reaches 30-45 percent.

Differentiation of tuberculous infiltrate is carried out with malignant neoplasms, with echinococcus and actinomycosis, lymphogranulomatosis, dermoid cysts, syphilis of the lung and other diseases. Only a thorough examination allows you to accurately recognize the nature of the process in the lungs.

Treatment of infiltrative pulmonary tuberculosis

Therapy for infiltrative tuberculosis is carried out in a hospital. Antibacterial drugs are used in combination with pathogenetic therapy. Treatment continues until the infiltrative changes have completely resolved - about nine to twelve months. In the future, chemotherapy courses are carried out to prevent relapses - already at a dispensary.

Various methods of treatment are used in combination. If the effect does not persist for a long time, in some cases, collapse therapy (artificial pneumothorax) is performed or a surgical operation is performed.

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Prevention of infiltrative pulmonary tuberculosis

Being a social disease, tuberculosis is often provoked by certain conditions of the patient's life. In Russia, the reasons for the deterioration of the epidemiological situation for tuberculosis include a decrease in the standard of living of the population, an increase in the number of people without a specific place of residence, and the development of migration. According to statistics, men are more likely to get sick - three point two tenths more than women. And among men, the incidence rate is growing two and a half times faster than among women. Most of the patients are twenty to twenty nine years old, in second place in terms of incidence is the group of thirty to thirty nine years.

People who are in prison get sick forty-two times more often than the rest of the country's population on average.

In order to prevent, it is necessary to carry out the following measures:

• Anti-epidemic measures that correspond to the extremely unfavorable tuberculosis picture in the country;
• Detection of cases at the first stages and financing of drug supply;
• Regular examinations of people who get a job in animal husbandry enterprises, where tuberculosis is observed among cattle;
• Allocation of isolated housing for people with active tuberculosis living in communal apartments and hostels;
• vaccination of newborns in the first thirty days of life.

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Which doctor should I contact?

In case of suspicion of infiltrative pulmonary tuberculosis, you should contact a phthisiatrician or pulmonologist.

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The author of the article: Makarova Evgenia Vladimirovna, pulmonologist