Tuberculosis - Information Overview

Tuberculosis is a disease that occurs when infected with microorganisms of the genus Mycobacteria, which make up the Mycobacterium tuberculosis complex. This complex includes several types of mycobacteria Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium africanum (the first two types are the most pathogenic microorganisms).

One bacteria carrier can infect an average of 10 people per year. The likelihood of infection increases in the following situations:

• upon contact with a patient with tuberculosis with massive bacterial excretion;
• in case of prolonged contact with a carrier of bacteria (living in a family, being in a closed institution, professional contact, etc.);
• in close contact with a carrier of bacteria (being in the same room with a sick person, in a closed group).

After infection with mycobacteria, clinically expressed disease may develop. The probability of developing the disease in a healthy infected person throughout life is about 10%. The development of tuberculosis depends primarily on the state of the human immune system (endogenous factors), as well as on repeated contact with mycobacteria tuberculosis (exogenous superinfection). The probability of developing the disease increases in the following situations:

• in the first years after infection:
• during puberty;
• in case of re-infection with Mycobacterium tuberculosis:
• in the presence of HIV infection (the probability increases to 8-10% per year);
• in the presence of concomitant diseases (diabetes mellitus, etc.):
• during therapy with glucocorticoids and immunosuppressants.

Tuberculosis is not only a medical and biological problem, but also a social one. Psychological comfort, socio-political stability, material standard of living, sanitary literacy, general culture of the population, housing conditions, availability of qualified medical care, etc. are of great importance in the development of the disease.

The role of primary infection, endogenous reactivation and exogenous superinfection

Primary tuberculosis infection occurs when a person is initially infected. As a rule, this causes adequate specific immunity and does not lead to the development of the disease.

In case of exogenous superinfection, repeated penetration of tuberculosis mycobacteria into the body and their reproduction are possible.

With close and prolonged contact with a bacteria carrier, mycobacteria tuberculosis repeatedly and in large quantities enter the body. In the absence of specific immunity, early massive superinfection (or constant re-infection) often causes the development of acutely progressive generalized tuberculosis.

Even in the presence of specific immunity developed after the primary infection, late superinfection can also contribute to the development of the disease. In addition, exogenous superinfection can contribute to the exacerbation and progression of the process in a patient with tuberculosis.

Endogenous reactivation of tuberculosis occurs from primary or secondary foci in organs that have remained active or have become aggravated. Possible causes are decreased immunity due to background or aggravated concomitant diseases. HIV infections, stressful situations, malnutrition, changes in living conditions, etc. Endogenous reactivation is possible in the following categories of people:

• in an infected person who has never previously had any signs of active tuberculosis:
• in a person who has had active tuberculosis and is clinically cured (once infected, a person retains tuberculosis mycobacteria in the body for life, i.e. biological cure is impossible);
• in a patient with a dying down tuberculosis process.

The possibility of endogenous reactivation in infected individuals allows tuberculosis to maintain a reservoir of infection even with clinical cure of all contagious and non-contagious patients.

Tuberculosis: epidemiology

According to WHO, tuberculosis affects nine million people worldwide every year, and more than two million die from it, with 95% of tuberculosis patients living in developing countries. In developed European countries, tuberculosis incidence has increased by 20-40% over the past decade (due to immigrants), while a decrease in the prevalence of this disease is recorded among the native population.

In Russia at the beginning of the 20th century, the mortality rate from tuberculosis was approximately the same as in European countries. Subsequently, a gradual decrease in mortality was observed. However, during the last century, four periods were noted, characterized by a sharp increase in mortality and a worsening of the epidemic situation: World War I, the Civil War, industrialization (1930s), the Great Patriotic War. The fourth period began with the collapse of the USSR and developed against the backdrop of an economic crisis. From 1991 to 2000, tuberculosis incidence increased from 34 to 85.2 cases per 100,000 people (in the USA this figure is 7). During this period, an increase in the mortality rate was also recorded, from 7.4 to 20.1 cases per 100,000 people. One of the reasons for the sharp deterioration of the epidemic situation in the country is considered to be the migration of the population from the republics of the former USSR. The prevalence of tuberculosis among migrants is 6-20 times higher than that among the native population. Currently, the mortality rate from tuberculosis in developed European countries is 10-20 times lower than in Russia, 40 times lower in Germany, and 50 times lower in the USA.

Symptoms of tuberculosis

It should be borne in mind that most phthisiologists understand intensive therapy of tuberculosis as intensive chemotherapy regimens for the disease, for example, treatment with not three, but five or more anti-tuberculosis drugs simultaneously. Currently, there is no clear definition of the concept of intensive therapy for tuberculosis. According to the current widespread opinion, an anesthesiologist-resuscitator should primarily perform correction and treatment of such complications of tuberculosis as respiratory and cardiac failure, pulmonary hemorrhage, and also master the methods of intensive preoperative preparation and methods of monitoring a patient suffering from tuberculosis during the early postoperative period. In our country, chemotherapeutic drugs are traditionally prescribed by a phthisiologist.

Clinical forms of pulmonary tuberculosis

There are several forms of tuberculosis, they are characterized by various complications, therefore the doctor of the intensive care unit must have minimal information about the variety of clinical forms of tuberculosis. However, traditionally, the treatment of complications is performed by anesthesiologists-resuscitators. It should be noted that the description of some clinical forms is shortened (due to their low significance for the intensive care physician).

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Disseminated pulmonary tuberculosis

This form of the disease is characterized by the formation of multiple tuberculous foci of productive inflammation in the lungs, formed as a result of hematogenous, lymphohematogenous or lymphogenous dissemination of mycobacterium tuberculosis. In case of hematogenous dissemination, foci are found in both lungs. If ineffective (or inadequate) treatment is carried out, the disease develops into chronic disseminated pulmonary tuberculosis with subsequent development of sclerosis, massive fibrosis and emphysema.

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Focal pulmonary tuberculosis

Focal pulmonary tuberculosis is characterized by the appearance of a few foci measuring 2-10 mm. A distinctive feature of this form of the disease is a small number of clinical symptoms. Focal tuberculosis is considered a minor form of tuberculosis. As a result of treatment, the foci resolve or turn into scars. When old foci become aggravated, their calcification is noted.

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Infiltrative pulmonary tuberculosis

The formation of caseous foci that spread to segments (or lobes) of the lung occurs with infiltrative tuberculosis. Often, this form of the disease is prone to an acute and progressive course. With adequate treatment, infiltrates can regress with restoration of the structure of the lung tissue. Sometimes, despite proper treatment, connective tissue compactions form at the site of infiltrates.

Caseous pneumonia

Caseous pneumonia is considered the most severe form of tuberculosis. This disease is characterized by an acute, progressive course and high mortality, reaching 100% in the absence of treatment. In the lungs, zones of caseous necrosis with lobar or multiple lobular lesions are determined. A distinction is made between lobar and lobular caseous pneumonia. With effective treatment, fibrous-cavernous pulmonary tuberculosis develops at the site of pneumonia.

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Tuberculoma of the lungs

Pulmonary tuberculoma is a capsulated caseous focus with a diameter of more than 1 cm. This form of the disease is characterized by an asymptomatic (or low-symptom) chronic course. Among all patients with detected round formations in the lungs, tuberculoma is diagnosed slightly less often than peripheral cancer. This form of the disease is not considered the cause of death of patients from tuberculosis.

Cavernous tuberculosis

Cavernous pulmonary tuberculosis is detected by the presence of an air cavity in the lung, with no inflammatory or fibrous changes in the wall. Clinical symptoms are usually mild.

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Fibrocavernous tuberculosis

Fibro-cavernous tuberculosis is characterized by the presence of chambers in the lungs with pronounced fibrosis of not only the wall, but also the surrounding tissues, as well as the formation of numerous foci of seeding. Fibro-cavernous tuberculosis is typically characterized by a long (with outbreaks or continuous) progressive course. This clinical form of the disease (and complications) is one of the main causes of death in patients suffering from pulmonary tuberculosis.

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Cirrhotic pulmonary tuberculosis

In cirrhotic pulmonary tuberculosis, massive fibrosis of the lungs and pleura and the presence of active and healed tuberculous foci are noted. Cirrhosis is the result of deforming sclerosis of the lungs and pleura. Pneumogenic cirrhosis, as a rule, occurs as an outcome of fibrous-cavernous tuberculosis. Patients suffering from this clinical form of the disease usually die from pulmonary heart failure, pulmonary hemorrhage and amyloidosis of internal organs.

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Tuberculous pleurisy and pleural empyema

Tuberculous pleurisy is an inflammation of the pleura with subsequent exudation into the pleural cavity. It may occur as a complication of pulmonary tuberculosis or tuberculosis of other organs. The disease includes three clinical forms: fibrinous (dry) pleurisy, exudative pleurisy, and tuberculous empyema. Sometimes tuberculous pleurisy occurs as an independent disease (without symptoms of tuberculosis of other organs), in which case pleurisy is the first sign of tuberculosis infection. With pleural tuberculosis, serous-fibrinous or hemorrhagic pleural effusion is detected. With destructive forms of pulmonary tuberculosis, the cavity perforates into the pleural cavity, where the contents of the cavity enter. Then the pleural cavity becomes infected and, as a result, empyema forms. Patients with pleural empyema are often diagnosed with pulmonary heart failure, respiratory failure, and amyloidosis of internal organs.

In developed countries, tuberculous empyema of the pleura is considered a casuistic form. Most often, this disease is registered in developing countries. Thus, one Chinese study was devoted to the analysis of pleural effusions and empyema of the pleura in patients (175 cases were considered) admitted to the intensive care unit. As a result, only three patients (out of 175) were found to have mycobacterium tuberculosis during microbiological testing.

The listed diseases are far from a complete list of clinical forms of pulmonary tuberculosis. Sometimes tuberculosis of the bronchi, trachea, larynx, tuberculous lymphadenitis and other conditions are diagnosed, which much less often require professional intervention of an intensive care physician.

Tuberculosis of the central nervous system

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Tuberculous meningitis

Cases of tuberculous meningitis are registered quite rarely in developed countries. For example, in the USA no more than 300-400 cases are registered per year. Without adequate treatment, most patients die within 3-8 weeks. With treatment, the mortality rate is 7-65%. Tuberculous meningitis is diagnosed in both children and adults. As a rule, the disease occurs in patients with pulmonary tuberculosis or tuberculosis of other organs. However, there are references to meningitis as the only clinical manifestation of the tuberculous process. Often, the inflammatory process spreads from the membranes not only to the brain substance (meningoencephalitis), but also to the substance of the spinal cord membrane (spinal meningitis).

Subfebrile temperature and general malaise are the first symptoms of tuberculous meningitis. Then hyperthermia (up to 38-39 °C), increasing intensity of headaches (due to the formation of hydrocephalus), and vomiting are noted. Some patients develop meningeal symptoms. Sometimes the disease begins acutely - with high temperature and the appearance of meningeal symptoms. Such a clinical picture is usually observed in children. In the absence of adequate treatment, stupor and coma occur, after which patients usually die.

When performing a blood test, leukocytosis with a band shift is noted, sometimes the number of leukocytes corresponds to the norm. Lymphopenia and an increase in ESR are characteristic.

In the diagnosis of tuberculous meningitis, CSF examination is of great importance. Cytosis (increased content of cellular elements) with a predominance of lymphocytes (100-500 cells/μl) and an increase in protein content to 6-10 g/l (due to coarsely dispersed fractions) are detected. A decrease in the amount of chlorides and glucose is recorded. In tuberculous meningitis, fibrin deposition (in the form of a mesh or herringbone) is noted in the CSF removed in a test tube after 24 hours. If a spinal puncture was performed before the start of specific therapy, tuberculosis mycobacteria are sometimes detected in the fluid (in less than 20% of cases). Enzyme immunoassay of CSF allows detection of anti-tuberculosis antibodies (in 90% of cases).

Tuberculous meningitis requires long-term treatment for 9-12 months. In addition to specific anti-tuberculosis therapy, glucocorticoid drugs are prescribed. It is believed that taking glucocorticoids for a month and then gradually reducing the dose of drugs can reduce the likelihood of developing remote neurological complications and their number. These drugs have a particularly good effect in children. If signs of hydrocephalus are detected, dehydration therapy is prescribed, lumbar punctures are performed to remove 10-20 ml of CSF. In severe intracranial hypertension, surgical decompression is recommended. Neurological complications occur in 50% of surviving patients.

Tuberculoma of the brain

Tuberculoma of the brain is most often diagnosed in children and young patients (up to 20 years). The disease develops in patients with tuberculosis of various organs or with tuberculosis of the intrathoracic lymph nodes, but in some patients, tuberculoma of the brain occurs as the only clinical form. The localization of tuberculomas is varied - they are found in any area of the brain. This disease is characterized by a wave-like course with remissions. Tuberculoma occurs against the background of prolonged subfebrile condition. Headache, nausea and vomiting are noted, meningeal symptoms are often determined. The severity and presence of neurological symptoms depend on the localization of the tuberculoma

On conventional radiographs, tuberculoma is mainly determined by the deposition of calcium salts in it. Therefore, the main method for diagnosing tuberculoma is considered to be computed tomography and magnetic resonance imaging.

Treatment is surgical only. Surgical intervention is performed against the background of taking anti-tuberculosis drugs during the entire preoperative and postoperative period.

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Cardiovascular tuberculosis

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Tuberculous pericarditis

In countries with a low incidence of tuberculosis, this clinical form is considered a severe but rare complication, occurring more often in the elderly and patients with HIV infection. In Russia, tuberculous pericarditis is registered quite often according to pathological studies, the involvement of the heart in the pathological process is found in 1.1-15.8% of patients who died from pulmonary tuberculosis. Sometimes pericarditis is the first clinical sign of tuberculosis. However, as a rule, pericarditis is diagnosed in combination with tuberculosis of other organs. Often, damage to the pleura and peritoneum (polyserositis) is noted.

The disease typically has a subacute onset, masked by clinical symptoms of tuberculosis with fever, dyspnea, and weight loss. In some cases, the disease debuts acutely and is accompanied by chest pain and pericardial friction rub. Pericardial effusion is almost always detected; in severe cases, cardiac tamponade develops. When examining the exudate (mainly of a hemorrhagic nature), a large number of leukocytes and lymphocytes are found in it, and in 30% of cases, tuberculosis mycobacteria. Biopsy allows for the diagnosis of tuberculous pericarditis in 60% of cases.

To establish an accurate diagnosis, X-ray diagnostics, CT and ultrasound are of great importance.

The main method of treatment is chemotherapy, but sometimes they resort to surgery and opening the pericardium.

In addition to the pericardium, tuberculosis often involves the myocardium, endocardium, epicardium, aorta and coronary arteries in the pathological process.

Osteoarticular tuberculosis

Bone and joint tuberculosis is a disease that affects any part of the skeleton. The most common localizations are the spine, hip, knee, elbow and shoulder joints, as well as the bones of the hands and feet. It occurs as a result of lymphohematogenous spread of infection. The process can spread to surrounding bone and soft tissues and cause the development of abscesses and fistulas.

The main methods of treatment are specific chemotherapy and surgical interventions aimed at removing the source of infection and restoring the function of bones and joints.

Urological tuberculosis

As a result of hematogenous or lymphohematogenous spread of infection, the kidneys, ureters, or bladder are affected. Renal tuberculosis (often combined with tuberculosis of other organs) is a sign of generalized tuberculous infection. When renal tissue is destroyed, a cavity is formed that opens into the pelvis. New cavities of decay appear around the cavity, followed by the formation of polycavernous tuberculosis. Later, the process often spreads to the pelvis, ureters, and bladder. Treatment is specific chemotherapy and surgical interventions.

Abdominal tuberculosis

For many decades, the disease was diagnosed quite rarely, so some specialists classify abdominal tuberculosis (along with caseous pneumonia) as relict forms. However, in the last 10-15 years, a sharp increase in the prevalence of this pathology has been noted. First of all, the mesenteric lymph nodes are affected and tuberculous mesadenitis is formed. The spread of the process to other groups of lymph nodes of the abdominal cavity, as well as to the peritoneum, intestines and pelvic organs is often recorded. In chronic forms, calcification of the lymph nodes is often noted. As a rule, tuberculous peritonitis, sometimes occurring as an independent disease, is a complication of generalized tuberculosis or tuberculosis of the abdominal organs. Intestinal tuberculosis also sometimes develops as an independent disease, but it is mainly detected with the progression of tuberculosis of the intra-abdominal lymph nodes or other organs. Tuberculous ulcers of the intestine can cause perforation of its wall.

Laparoscopy with biopsy of areas suspected of tuberculosis is of great importance for establishing a diagnosis.

Treatment is long-term (up to 12 months) chemotherapy. Surgical treatment is usually performed when complications of abdominal tuberculosis develop, such as intestinal obstruction, perforation of tuberculous ulcers.

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Other clinical forms of tuberculosis

Other clinical forms of the disease, such as tuberculosis of the genitals, skin, and eyes, are of lesser importance to the intensive care physician.

Classification of tuberculosis

• Pulmonary tuberculosis
  • Disseminated pulmonary tuberculosis
  • Focal pulmonary tuberculosis
  • Infiltrative pulmonary tuberculosis
  • Caseous pneumonia
  • Tuberculoma of the lungs
  • Cavernous tuberculosis
  • Fibrocavernous tuberculosis
  • Cirrhotic pulmonary tuberculosis
  • Tuberculous pleurisy and pleural empyema
  • Tuberculosis of the bronchi
  • Tuberculosis of the trachea
  • Tuberculosis of the larynx
  • Tuberculous lymphadenitis
• CNS tuberculosis
  • Tuberculous meningitis
    • Tuberculous meningoencephalitis
    • Spinal form of tuberculous meningitis
  • Tuberculoma of the brain
• Cardiovascular tuberculosis
  • Tuberculous pericarditis
• Tuberculosis of the bones and joints
• Urological tuberculosis
• Abdominal tuberculosis
  • Other clinical forms of tuberculosis
    • Tuberculosis of the genital organs
    • Lupus
    • Tuberculosis of the eye

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Treatment of tuberculosis

The main method of treating tuberculosis of various localizations is considered to be chemotherapy. Its therapeutic effect is due to the antibacterial action and is aimed at suppressing the reproduction of mycobacteria or destroying them (bacteriostatic and bactericidal effect). Rifampicin, streptomycin, isoniazid, pyrazinamide and ethambutol are the main anti-tuberculosis drugs.

Reserve drugs are used to treat drug-resistant forms of tuberculosis. These include kanamycin, capreomycin, amikacin, cycloserine, fluoroquinolones, ethionamide, prothionamide, rifabutin, and aminosalicylic acid (PAS). Some drugs (e.g., rifampicin, fluoroquinolones, ethambutol, cycloserine, and prothionamide) have the same activity against intracellular and extracellular mycobacteria tuberculosis. Capreomycin and aminoglycosides have a less pronounced effect on mycobacteria localized inside cells. Pyrazinamide has a relatively low bacteriostatic activity. However, the drug enhances the effect of many drugs, penetrates well into cells, and produces a significant effect in the acidic environment of caseose.

The standard treatment regimen consists of the combined administration of rifampicin, isoniazid, pyrazinamide and ethambutol (or streptomycin). In our country, with its well-developed phthisiology service, the phthisiologist traditionally determines the regimens, methods and duration of chemotherapy.

It is interesting to know that the world's first randomized study was conducted in phthisiology. In 1944, streptomycin was obtained in the United States. In 1947-1948, the first study was conducted in Great Britain involving tuberculosis patients. The control group consisted of patients who observed bed rest, the main group consisted of patients who additionally received streptomycin. However, the study used an insufficient amount of the drug, and its effectiveness had not yet been definitively proven. Due to the small amount of streptomycin, the study was considered ethically acceptable.

As studies have shown, the use of streptomycin in the treatment of pulmonary tuberculosis allows to reduce mortality from 26.9% in the control group to 7.3% in the group of patients who used streptomycin. In fact, this statement can be considered the birthday of not only evidence-based medicine, but also modern chemotherapy of tuberculosis.