Lecture No. 16. Tuberculosis

Etiology. Tuberculosis is caused by tuberculosis bacilli belonging to the Mycobacterium family, a group of actinomycetes. In humans, the leading role is played by M. tuberculosis, which is responsible for the majority of cases of the disease; M. bovis is the causative agent of tuberculosis in cattle and rabbits; M. avium causes disease in birds and white mice. All mycobacteria are nonmotile, aerobic, non-spore forming polymorphic rods. They are difficult to stain due to the high lipid content in their cell wall, but once they take on color, they are no longer discolored by alcohol and acids. A feature of Mycobacterium tuberculosis is its very slow growth on nutrient media (on average, a response is obtained after 21 days). Under the influence of various environmental factors, the causative agent of tuberculosis exhibits a wide range of variability in the morphology of bacterial cells - from the smallest filterable particles and grains to giant branched forms, which affects their functional properties. Mycobacterium tuberculosis may develop resistance to all specific antibiotics and chemotherapy drugs, which prevents effective treatment of the disease.

Epidemiology. Tuberculosis is a relatively common disease; the main sources of infection in children are adults with active tuberculosis and cattle affected by tuberculosis.

The most dangerous are patients with bacterial excretion. The main route of infection transmission is airborne. The rest - alimentary, contact, through damaged skin and mucous membranes - are rare and do not have great epidemiological significance.

Immunology. Immune reactions in tuberculosis are a complex set of interactions between the pathogen, special populations of lymphocytes and tissue macrophages. Various types of antibodies produced during the development of infection do not play a significant role in suppressing the growth of mycobacteria and in the development of anti-tuberculosis immunity. Cellular immune responses begin to appear after live and pathogenic mycobacteria enter the body. Pulmonary macrophages phagocytose them, but are unable to destroy them. The pathogen continues to multiply in macrophages, and with them mycobacteria enter the regional lymph nodes. Subsequently, the infection spreads through hematogenous and lymphogenous routes with the formation of numerous extrapulmonary foci.

Immunological processes are completed within 6-10 weeks, leading to the development of primary infection and elimination of metastatic foci.

The development of natural immunity to this life-threatening infection depends on the influence of:

1) genetic factors that have a certain influence on the development of the disease and its outcome;

2) age, which determines the severity of tuberculosis infection. Children under 3 years of age are most often prone to miliary tuberculosis and meningitis with a fatal outcome;

3) factors affecting the function of T-lymphocytes and thereby contributing to the development of severe forms of the disease: malnutrition, various infections, primarily measles and whooping cough, pregnancy, diseases of the reticuloendothelial system, lymphocytic leukemia. The appointment of immunosuppressive drugs, in particular corticosteroids, may contribute to the development of particularly severe forms of primary tuberculosis infection or the reactivation of a dormant infection.

Diagnostic skin tests. Skin reactions to the administration of tuberculin are based on the detection of delayed-type hypersensitivity to antigens of tuberculous mycobacteria and are of great importance in the diagnosis of tuberculosis infection. Positive reactions appear 6-10 weeks after pathogens enter the body. The test involves intradermal injection of an antigen drug into the patient. A positive reaction is expressed by the appearance of indurate at the injection site. It is caused by migration of activated lymphocytes and macrophages to the area of ​​antigen injection. Two different tuberculin preparations are used: old Koch tuberculin (alt-tuberculin, ATK) and purified protein-free tuberculin PPD. ATK is a crude product obtained by sterilizing the filtrate of a culture on which tuberculous mycobacteria were grown. This drug is used only in a multiple skin prick test.

For all tuberculin skin tests, including the Mantoux test and the multiple puncture test, tuberculin PPD is preferred.

Mass screening of tuberculosis infection in pediatric practice is carried out using multiple puncture methods. The disadvantage of this relatively sensitive method is the weak specificity, therefore, in cases of a positive or doubtful reaction, it is usually necessary to additionally examine using the Mantoux test. The most common is the Tine-test, which involves the use of a plate with four steel spikes soaked in ATK. The test results are taken into account after 48-72 hours. A positive reaction is expressed by the appearance of vesicles or more often papules with a size of at least 2 mm at the site of one or more punctures. The Apli-test is performed using tuberculin PPD with phenol.

The Heaf test involves the use of a special device that simultaneously produces 6 skin punctures to a depth of 1 mm through a layer of concentrated PPD tuberculin. The sample can be taken into account within the next 3-7 days. A positive reaction is expressed by the appearance of 4 or more papules at the puncture site. False positive reactions are not uncommon with all multiple puncture techniques. In addition, all positive and doubtful reactions require confirmation of the Mantoux test.

The Mantoux test is more complex than multiple puncture methods, but more accurate, since it introduces a strictly defined amount of antigen. The results of the reaction are taken into account after 48-72 hours. The appearance of an indurat with a diameter of 10 mm at the injection site indicates an infection with tuberculosis and is regarded as a positive reaction.

With an indurate of 5 to 10 mm, the reaction is regarded as doubtful, and with an indurate diameter of up to 5 mm, as negative. In the latter case, it is necessary to exclude the possibility of allergy, for example, by conducting skin allergy tests to infectious mumps allergens (after vaccination) or to Candida antigens.

Questionable reactions to tuberculin are most often associated with infection with atypical mycobacteria, since tuberculin PPD contains antigens that are common with antigens of non-tuberculous mycobacteria. Cross-reactions are most often observed with the introduction of large doses of tuberculin (250 IU).

Under certain circumstances, an indurat of 5 to 10 mm can be interpreted as a dubious reaction and treatment can be prescribed. False-negative results of the Mantoux test can occur for many reasons: they are negative in the early stages of the disease, even with the introduction of 250 IU; as a result of technical errors in the storage of tuberculin and during the test; as a result of the suppression of tuberculin reactions by preventing activation by lymphocytes and the development of delayed-type hypersensitivity (due to infancy, severe diseases of any type, intercurrent infections of viral etiology, administration of an attenuated viral vaccine, immunosuppressive therapy, malnutrition, neoplastic processes, sarcoidosis, chronic renal failure) .

False-positive results of the Mantoux test can be observed with repeated injections of tuberculin PPD or ATK, as well as after BCG vaccination. BCG vaccination leads to positive tuberculin reactions, which are difficult to distinguish from reactions that occur with tuberculosis infection. Any reaction to intradermal administration of tuberculin larger than 10 mm, occurring 3 years or more after BCG vaccination, should be considered as an indicator of tuberculosis infection.

Clinical forms of tuberculosis

1. Intrathoracic tuberculosis

Pathogenesis and pathomorphology. Primary infection most often develops after inhalation of live virulent tuberculous mycobacteria. The body of a non-immune child reacts to infection with certain cellular reactions. Pathogens are phagocytosed by macrophages, their further reproduction occurs in these cells, and macrophages carry mycobacteria into regional lymph nodes. Subsequently, lymphogenous and hematogenous dissemination of the infection occurs with the appearance of metastatic foci in the lungs, in the reticuloendothelial system and in other organs.

During this period, when cellular immunity reactions to tuberculosis infection have not yet developed, tissue damage is minimal, and clinical symptoms may be absent. In the vast majority of cases, acquired immunity reactions form 6-10 weeks after infection and are accompanied by recovery, calcification of pulmonary and extrapulmonary foci occurs. Dormant tuberculous infection persists in these residual tuberculous changes, usually located in the apical and subapical regions of the lungs.

Any factors that damage the response of cellular immunity can lead to the reactivation of tuberculosis infection, to the multiplication of pathogens in these foci and the development of pulmonary or extrapulmonary lesions. In contrast to the primary infection, reactivation, or, as it is also called, post-primary tuberculosis or "adult tuberculosis", occurs against the background of pronounced reactions of cellular immunity. Most often, it is localized and is accompanied by severe symptoms and tissue lesions.

Primary pulmonary tuberculosis

Clinical manifestations. In children aged 3 to 15 years, primary tuberculosis is usually asymptomatic, may not be accompanied by changes on chest x-rays and manifests itself only by changes in tuberculin tests. General symptoms can be mild and nonspecific, manifesting themselves as slight increases in temperature, loss of appetite, weight loss, and less commonly erythema nodosum and phlyctenular conjunctivitis.

Additional symptoms may develop later with a massive increase in intrathoracic lymph nodes, characteristic of a primary tuberculosis infection. In these cases, the enlarged lymph nodes are displaced, squeezed, impair patency or destroy various adjacent organs of the mediastinum. In most children, primary lung infection is mild, asymptomatic, and resolves within a short time even without chemotherapy.

In older children and adolescents, primary pulmonary tuberculosis usually manifests itself as pronounced infiltrative changes in the upper parts of the lungs with the development of destruction, while there are no signs of calcification and enlargement of the intrathoracic lymph nodes. Less commonly, there is a lesion of the middle and lower parts of the lungs with involvement of the intrathoracic lymph nodes, which is characteristic of young children. In younger children, against the background of the described symptoms, a picture of lympho- and hematogenous dissemination may develop, leading to miliary tuberculosis and meningitis.

Diagnosis. Primary pulmonary tuberculosis is diagnosed in children during examination regarding the incidence of tuberculin tests. The diagnosis of tuberculosis requires bacteriological confirmation.

2. Progressive primary pulmonary tuberculosis

In some cases, the primary focus formed in the lungs does not heal, but increases in size. Damage to the entire lower or middle lobe of the lung may develop. Typically, this course of the disease is observed in patients with suppressed immunity. The increase in intrathoracic lymph nodes in such patients is natural, endobronchial spread of infection and the development of destructive changes in the lungs are often observed. Clinical symptoms are pronounced: febrile body temperature, malaise, anorexia, weight loss, cough with sputum. Physical examination and radiographs reveal hilar adenopathy, inflammatory changes in the middle or lower lobes of the lungs, and cavern formation. The diagnosis must be confirmed by bacteriological data.

3. Reactivation (reinfection) of tuberculosis

Reactivation of tuberculosis (or "adult" tuberculosis) is not typical for childhood, especially with the development of primary tuberculosis at the age of about 3 years. Lesions in these cases are localized in the apical and dorsal segments of the upper lobes or in the apex of the lower lobe. An increase in hilar lymph nodes is rare. The most characteristic symptom is subfebrile temperature and night sweats due to a decrease in temperature. Additional symptoms: malaise, weakness, weight loss. The development of caseous necrosis, its melting and emptying with the formation of cavities are manifested by a cough with sputum, often with a slight hemoptysis. On physical examination, gentle rales are found predominantly in the apical regions of the lungs, especially after coughing. The earliest radiographic findings are usually homogeneous, well-demarcated opacities at the apex of the lungs. With an increase in infiltrative changes, lesions of the lobar length may occur. After melting and rejection of caseous necrosis, classical thin-walled cavities are formed, sometimes with a liquid level in them.

4. Pleural effusion

The development of pleurisy can occur as a result of the penetration of tuberculosis mycobacteria into the pleural cavity from peripherally located tuberculosis foci in the lung, as a result of hematogenous dissemination of the pathogen.

It is bilateral, accompanied by pericarditis and peritonitis. Often these lesions resolve spontaneously. Often, a few years after suffering pleurisy, patients observe reactivation of pulmonary tuberculosis. Such patients are shown prophylactic administration of anti-tuberculosis drugs.

The differential diagnosis of tuberculous pleurisy should be carried out with pleural effusions due to heart failure, malignant neoplasms, malnutrition and metabolism, with collagen vascular lesions and parapneumonic nonspecific pleurisy due to other infections. Pleural effusion in tuberculous pleurisy is characterized by a significant specific gravity, high protein content, increased activity of lactate depidrogenase and adenosine deaminase, and low glucose levels. In a cytological examination, neutrophils can be detected in it in the early stages, lymphocytes predominate, mesothelial cells are usually absent. Mycobacterium tuberculosis in the pleural effusion with bacterioscopy usually cannot be detected, but when sowing exudate and pleural tissue, pathogens are detected in almost half of the cases. With repeated punctures and centrifugation of the removed fluid, the effectiveness of the seeding method increases. A biopsy of the pleura should be performed in all cases and preferably at the same time as the first pleural puncture. In the absence of effusion in the pleural cavity, pleural biopsy is difficult. Histological examination of the pleural biopsy material in most cases reveals granulomatous changes. The appearance of pleural effusion in children with positive tuberculin reactions in all cases should raise the suspicion of tuberculosis and serve as the basis for an appropriate examination. Similarly, pleurisy of unknown etiology in a child with negative tuberculin tests requires a repeat tuberculin diagnosis after 2-3 weeks. Under normal conditions, nonspecific pleural effusion quickly resolves, thoracocentesis and drainage are not indicated.

5. Extrathoracic tuberculosis

Tuberculosis of the upper respiratory tract. Tuberculosis of the larynx in a child almost always occurs against the background of cavernous pulmonary tuberculosis, its symptoms are persistent cough, sore throat and pain when swallowing, hoarseness of voice. Tuberculosis of the middle ear is accompanied by hearing loss, diffuse otorrhea, absence of pain and enlargement of the parotid lymph nodes. Often, there are violations of the facial nerve and signs of mastoiditis. Otoscopy reveals thickening of the tympanic membrane and its perforation in one or more places. Treatment of upper respiratory tract tuberculosis depends on the extent of the pulmonary lesion. Isoniazid and rifampicin are usually indicated for 18-24 months. Surgical interventions are indicated for the development of paralysis of the facial nerve, with mastoiditis and with subperiosteal abscesses.

Tuberculosis of the lymph nodes. The defeat of peripheral and deep lymph nodes is considered a characteristic feature of tuberculosis infection.

In children, the hilar lymph nodes are most often affected first, from which the process can subsequently spread to paratracheal, supraclavicular, deep cervical or intraperitoneal groups of lymph nodes. The defeat of the axillary and inguinal lymph nodes is much less common and usually with the localization of the primary focus on the corresponding limbs.

Adenopathy sometimes develops as a result of hematogenous or lymphogenous dissemination of tuberculosis mycobacteria in the initial phase of primary tuberculosis infection before the development of specific immunity. In these cases, changes are found in the peripheral and deep groups of lymph nodes.

Tuberculosis of the peripheral lymph nodes is the most common of all extrapulmonary forms of tuberculosis, characterized by the localization of multiple, often bilateral lesions mainly in the neck.

Clinical manifestations. Tuberculosis of the lymph nodes usually begins gradually and unnoticeably. Only in children highly sensitive to tuberculosis infection is an acute onset of the disease with an increase in body temperature and the development of local signs of inflammation possible. The history often contains indications of contact with patients with active tuberculosis. Most children have positive tuberculin tests, and chest x-rays show signs of primary pulmonary tuberculosis. A significant increase in nodes and compression of neighboring organs is observed only in exceptional cases. Melting of enlarged surface nodes can lead to the spread of the process to surrounding tissues and the formation of external fistulas.

On palpation, the nodes are compacted, can be hard, not soldered to each other. Less often, when melted, they are soft and solder with surrounding tissues or with the skin. Sometimes fistulas are found.

Diagnosis and differential diagnosis. An accurate diagnosis is possible based on histological or microbiological examination. However, histological examination does not allow differentiating tuberculous lymphadenitis from lesions that occur when infected with atypical mycobacteria. Therefore, in all cases, it is advisable to send biopsy material for microbiological examination for inoculation on appropriate nutrient media.

Tuberculous lymphadenitis must be differentiated from non-tuberculous mycobacteriosis, diseases caused by viruses, fungi, toxoplasma, bacteria and the causative agent of cat scratch disease, as well as malignant lesions, sarcoidosis and reactions to certain drugs.

Treatment. Tuberculous lesions of the lymph nodes respond well to treatment with isoniazid and rifampicin or ethambutol, which are prescribed for a period of at least 18 months.

6. Miliary tuberculosis

Miliary tuberculosis occurs more often in children under 3 years of age with hematogenous dissemination of mycobacteria with the development of granulomas in many organs that undergo caseous necrosis. The development of miliary tuberculosis is facilitated by the presence of chronic diseases, immunosuppressive therapy and AIDS.

Clinical manifestations. The onset of the disease in children can be acute. Body temperature rises, weakness, malaise, anorexia, and weight loss develop. On physical examination, nonspecific changes are noted in the form of lymphadenopathy, enlargement of the liver and spleen. Subsequently, respiratory disorders increase in the form of shortness of breath, tachypnea, cough, and scattered wheezing in the lungs. With the development of meningitis, headaches, lethargy, and stiffness of the neck muscles occur. Metastatic skin lesions and the appearance of tuberculous tubercles in the fundus are rare symptoms of miliary tuberculosis.

In the case of periodic penetration of a small number of pathogens into the bloodstream, a picture of chronic hematogenous disseminated tuberculosis usually develops, which is more typical for adult patients, and not for children. Its clinical symptoms are short or long periods of fever, weakness, weight loss, increasing over a long time (weeks and months). As a rule, diffuse lymphadenopathy, enlargement of the liver and spleen are noted.

Diagnosis. Diagnostic methods are:

1) X-ray examination, in which diffuse widespread rashes of a characteristic type are determined in the lungs. But in the initial period of the disease, changes on radiographs are not yet visible, so the study should be repeated in case of the slightest suspicion of this disease;

2) cultures of blood, urine, gastric contents and cerebrospinal fluid in order to detect Mycobacterium tuberculosis;

3) transthoracic lung biopsy performed during bronchoscopy performed using fine-fiber optics in order to detect specific granulation tissue, sometimes with signs of caseous necrosis, as well as acid-fast bacilli.

Treatment. The use of isoniazid and rifampicin in combination with ethambutol or streptomycin is indicated. In severely ill patients with signs of respiratory failure and hypoxemia, corticosteroids are simultaneously recommended.

7. Tuberculous meningitis

Epidemiology. The incidence of tuberculous meningitis depends on the prevalence of tuberculosis in a given area. The disease most often develops within six months after infection with tuberculosis, so it is usually considered a childhood disease.

Pathophysiology and pathomorphology. Hematogenous generalization of infection, characteristic of this disease, leads to the formation of metastatic foci of tuberculosis infection. Solitary tuberculous foci (tuberculomas) can occur in the central nervous system; the membranes of the brain and spinal cord are affected. Tuberculous meningitis occurs when tuberculous tubercles, localized subependymal, or large tuberculous foci located near the meninges, break into the subarachnoid space, emptying their infected contents into it. In this case, a severe inflammatory reaction develops in the immune body, primarily from the central nervous system. Soon a thick gelatinous effusion appears, lining the basal surface of the brain in a thick layer, as a result of which the cerebral arteries and veins are compressed, the cranial nerves are damaged, and the basal cisterns and interventricular foramina are obliterated.

Clinical manifestations. Symptoms of the disease develop gradually. There are three stages of the process:

1) the prodromal phase, characterized by nonspecific symptoms: apathy, mood deterioration, poor school performance, loss of appetite, nausea, vomiting, and low-grade fever;

2) the stage of onset of clinical symptoms, which occurs after a couple of weeks and is characterized by the appearance of neurological symptoms. Irritability increases, older children complain of a headache. Neck stiffness may appear in combination with Kernig's and Brudzinski's symptoms. Loss of function of the cranial nerves is characteristic: pathology of pupillary reactions, diplopia, decreased visual acuity, hearing impairment, facial paralysis. Often there are speech disorders, aphasia, disorientation, hemiplegia, ataxia, involuntary movements and convulsions. Intracranial pressure at this stage of the disease is increased. At the same time, there may be an increase in the volume of the head, bulging of the fontanelles, and in older children - swelling of the nipple of the optic nerve;

3) the stage of impaired consciousness up to stupor and coma, characterized by an increase in signs of diffuse cerebral dysfunction. Stupor, coma, decerebration or decortication, irregular breathing, pupils fixed or dilated develop.

Diagnosis. In all doubtful cases, after a thorough and comprehensive study of the anamnesis and clinical examination, it is necessary to resort to a diagnostic spinal puncture, including counting cellular elements, determining the content of protein, sugar and chlorides, examining the cerebrospinal fluid for tuberculous mycobacteria, direct bacterioscopy using the flotation method or using cultures and infection of the guinea pig.

Treatment. It is recommended to prescribe isoniazid and rifampicin during the first 2 months of treatment with additionally prescribed streptomycin or ethambutol. Subsequently, treatment with isoniazid and rifampicin is continued for another 10 months.

Forecast. The outcome of tuberculous meningitis depends on the patient’s condition at the time of treatment. With treatment started in the 1st stage of the disease, cure occurs in all patients, and residual changes are minimal. Optimal results of treatment started in the 2nd stage of the disease are obtained in 85% of patients, and half of the survivors still have significant impairments. Treatment started in the 3rd stage of tuberculous meningitis saves the lives of only 50% of patients, and they usually remain severely disabled.

8. Tuberculoma of the central nervous system

Single or multiple tuberculomas can form at any stage of the course of tuberculosis infection and are manifested by symptoms of a slowly growing volumetric process in the brain. Headaches, increased intracranial pressure, visual disturbances are noted. On radiographs of the skull, signs of calcification in tuberculomas are occasionally found. Computed tomography in the early stages reveals contrasting shadows surrounded by an annular edema zone. In the anamnesis of sick children, there is usually information about contact with patients with active tuberculosis. Most of them also have tuberculous changes in the lungs in the form of hilar lymphadenopathy, infiltrative changes in the lower lobes, and pleurisy. Tuberculin reactions are positive.

Often, the diagnosis of brain tuberculoma is established only during surgery. Usually, treatment is carried out with three anti-tuberculosis drugs for 12-18 months. Corticosteroids are prescribed in the first weeks of treatment, mainly to reduce cerebral edema.

Chemotherapy for tuberculosis. Studies to determine the optimal duration of chemotherapy and the most effective anti-tuberculosis drugs in children show that simply transferring the principles of adult chemotherapy to pediatric practice can lead to “overtreatment” of children, since adults have to deal with a much larger bacterial population in cases of destructive tuberculosis.

In many cases, effective treatment of tuberculosis infection in children is possible on an outpatient basis. Hospitalization is recommended for:

1) the need for repeated cultures and biopsies to confirm the diagnosis;

2) severe, life-threatening processes to start treatment and select adequate therapy;

3) the selection of chemotherapy at the initial stage in infants and young children;

4) the need for surgery or corticosteroid therapy;

5) overcoming severe drug intolerance reactions;

6) concomitant diseases requiring inpatient treatment;

7) difficult domestic and social conditions that prevent adequate treatment at home.

In these cases, the transfer of a sick child to outpatient treatment can be carried out only after the establishment of therapy and the organization of subsequent monitoring of its implementation.

Anti-tuberculosis drugs. Isoniazid is the drug of choice for the treatment of all forms of tuberculosis; it is prescribed for all therapeutic regimens if the pathogens remain sensitive to it. Side effects of the drug are rare.

Rifampicin is a broad-spectrum antibiotic that is available for oral use and is prescribed in the most active phase of the tuberculous process once a day at a dose of 1-15 mg/kg. The side effect of the drug is expressed by orange staining of teeth, urine and saliva, symptoms of the gastrointestinal tract, toxic changes in the liver, especially in the first weeks of therapy. The risk of hepatotoxicity is greatest when rifampicin is given concomitantly with isoniazid. In these cases, the dose of the latter drug is recommended to be reduced to 20 mg/kg. Intermittent treatment with rifampicin often results in thrombocytopenia, leukopenia, and a flu-like syndrome.

Ethambutol has an effect only on mycobacteria. The drug is administered orally 1 time per day at a dose of 15-20 mg/kg. A side effect is expressed by reversible visual impairment - narrowing of the visual fields and a change in the perception of color. Ethambutol can serve as a substitute for isoniazid in combination with streptomycin in cases of isoniazid drug resistance. The use of ethambutol in young children is limited due to insufficient knowledge of its pharmacokinetics and difficulties in visual control at this age.

Streptomycin is significantly less effective against Mycobacterium tuberculosis than isoniazid and rifampicin, but is superior in this regard to ethambutol. In severe forms of tuberculosis, streptomycin is administered intramuscularly once a day at a dose of 1 mg / kg along with isoniazid and rifampicin during the first few months of therapy. Most often, the side effect is manifested by a violation of the function of the VIII pair of cranial nerves, especially their vestibular department.

The results of this action are ataxia, balance disorders and, less commonly, hearing loss.

Pyrazinamide, administered simultaneously with isoniazid, has a bactericidal effect on Mycobacterium tuberculosis. The drug is administered orally, its daily dose (30-40 mg / kg) is divided into 2-3 doses. The disadvantages of the drug are the tendency to more rapid development of drug resistance of the pathogen against the background of its administration, the hepatotoxic effect - sometimes provokes the development of jaundice.

Ethionamide has a pronounced effect on Mycobacterium tuberculosis, is prescribed in combination with other drugs in the treatment of relapses of the disease and the ineffectiveness of standard chemotherapy regimens. The drug is taken orally 1 time per day at a dose of 15 mg / kg. Side effects of ethionamide usually affect the gastrointestinal tract (such as nausea, vomiting, abdominal pain).

Monotherapy. Chemoprophylaxis with isoniazid is indicated for all practically healthy persons under 35 years of age with positive tuberculin tests, in whom no changes are detected on chest x-rays or where there are traces of previous tuberculosis. To prevent reactivation of the infection with the development of a general disease, such individuals are recommended to be treated for 12 months. Children at high risk of infection with isoniazid-resistant strains of the pathogen require careful follow-up along with isoniazid chemoprophylaxis. Preventive monotherapy with isoniazid can also be administered to children at high risk of tuberculosis. Treatment in such cases is prescribed even to children with a tuberculin-negative reaction. In usual practice, isoniazid is prescribed for 3 months and then tuberculin tests are repeated. If a turn occurs, treatment is continued for up to 12 months. If skin reactions to tuberculin remain negative, and the source of infection has already been eliminated during this time, then chemoprophylaxis is gradually completed. Lack of effect from chemoprophylaxis can be observed during infection with isoniazid-resistant strains of Mycobacterium tuberculosis.

Two- and three-drug treatment regimens. Most cases of tuberculosis in children respond well to treatment with a dual combination of anti-tuberculosis drugs. The most commonly used drugs are isoniazid and rifampicin, and less commonly, ethambutol. The duration of such therapy in children is 12 months. A triple combination of drugs (isoniazid, rifampicin and streptomycin) is indicated in the initial stages of treatment of children with the most severe, life-threatening forms of tuberculosis. In the presence of drug resistance to isoniazid, treatment is carried out with rifampicin, streptomycin and ethambutol.

Children with destructive bacillary forms of pulmonary tuberculosis stop excreting mycobacteria in sputum already 2 weeks after the start of treatment according to chemotherapy regimens with rifampicin. A longer period of isolation is necessary in cases where there is contact with healthy children or infection with resistant strains of the pathogen is suspected.

Prevention. Prevention of tuberculosis involves the following measures:

1) prevention of contact with patients with active forms of tuberculosis;

2) carrying out specific chemoprophylaxis;

3) BCG vaccination in high-risk groups;

4) general improvement of social and economic conditions.

The anti-tuberculosis vaccine is a preparation of live attenuated harmless mycobacteria of the BCG vaccine strain (Bacillus Calmette and Guerin) and is used as the most effective and economical intradermal method of vaccination. An important indicator of the quality and effectiveness of BCG vaccination is the post-vaccination reaction:

1) a local reaction during intradermal vaccination is characterized by the appearance of a small infiltrate with pink staining of the skin above it with a diameter of up to 12 mm. The infiltrate may look like a nodule with a cyanotic tinge; pustules - a slight enlightenment due to thinning of the skin over the infiltrate, which can dry out and resolve, or can be converted into a crust like smallpox; small ulceration with serous-purulent discharge, spontaneously healing. The described nature of the reactions is considered as normal, reflecting the individual reactivity of the organism. The reverse development of changes at the site of vaccination occurs within 2-4 months, less often - in longer periods. Superficial scars from 2 to 10 mm remain at the healing site;

2) post-vaccination allergy - an objective indicator of the immunological restructuring of the body under the influence of the BCG vaccine, develops in 50% of the Mantoux test.

Contraindications to vaccination of newborns: prematurity, intrauterine infection, purulent-septic diseases, hemolytic disease of the newborn, severe birth injuries with neurological symptoms, generalized skin lesions, acute diseases, generalized BCG infection in other family members.

Revaccination is contraindicated in children and adolescents infected with tuberculosis or who have had tuberculosis in the past, with a positive or questionable Mantoux test, who had complicated reactions to previous injections of the BCG vaccine, with malignant blood diseases and neoplasms, immunodeficiency conditions, treated with immunosuppressants, with acute diseases, with allergic diseases in the acute stage (vaccinated 1 month after recovery or remission on the conclusion of a specialist).

The frequency of post-vaccination complications is 0,02-0,03%.

Author: Muradova E.O.

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Random news from the Archive Electrons flow like a liquid 20.09.2017 In their latest experiments, scientists from the Graphene Institute at the University of Manchester have discovered conditions under which electrons moving through graphene behave in a very unusual way. This specific movement of electrons gives scientists a better understanding of the physical processes in electrically conductive materials, and in the near future, these same processes can be used to develop nanoelectronic circuits for fast and high-performance next-generation computer chips. In most metals, electrical conductivity is limited by the number of defects in their crystal lattice, which cause electrons to scatter, hitting them like billiard balls. Therefore, graphene, due to its "two-dimensional" structure, conducts electricity much better than any metal. In addition, in some pure metals and other materials with an ordered crystal structure, including graphene, electrons can overcome distances of microns without scattering due to the so-called ballistic motion. The parameters of such motion determine the maximum possible electrical conductivity of the material, which is called Landauer's fundamental limit. However, the data obtained during the experiments allowed scientists to conclude that the law that determines the fundamental Landauer limit is not observed in the graphene medium under certain conditions. And one very unusual mechanism is responsible for this, which is directly related to the relatively new field of physics called electron hydrodynamics (electron hydrodynamics). The field of electron fluid dynamics emerged just last year after scientists from the University of Manchester and other scientific organizations showed that at a certain temperature of a material, electrons moving in it begin to collide with each other so often that the flow of electrons begins to flow like a liquid flow, having not the smallest coefficient of viscosity. And in new research, scientists have shown that the presence of this viscous "e-liquid" gives the material a higher electrical conductivity than the ballistic movement of electrons. The phenomenon discovered by scientists is rather paradoxical. Indeed, during collisions of electrons, they interact and scatter, which, in theory, should weaken the electrical conductivity of the material. But the increase in the conductivity of the material occurs due to the fact that the electrons are divided into two conditional parts, like a stream of water flowing in a river. Those electrons that move in close proximity to the edges of the crystal lattice lose their momentum and slow down. But, at the same time, they act as a protection against collisions of electrons moving in the middle of the stream. And these electrons are already moving along a super-ballistic trajectory inside the "channel" created by the extreme electrons. “We know from school physics that the more disordered the structure of a material, the greater its electrical resistance,” says Sir Andrew Game, “But in our case, the disorder caused by scattering due to electron collisions reduces, rather than increases, the electrical resistance of the material. In this case, the electrons begin to flow like a liquid and the speed of this liquid exceeds the speed of electrons with the same energy in vacuum. The scientists conducted a series of experiments in which the conductivity of graphene was measured at various temperatures. Comparison of the conductivity of pure graphene and doped graphene, which has clear metallic conductive properties, allowed scientists to calculate with high accuracy a new physical quantity called viscous conductivity. And what is most remarkable, the collected experimental data practically coincided with the data obtained in the course of calculations of the corresponding mathematical models.

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