Pathogen and Nature of the Disease
Tuberculosis is a bacterial infectious disease caused by Mycobacterium tuberculosis (Koch's bacillus), transmitted primarily from person to person, as well as from animals. The pathogen has a characteristic rod-like shape and is detected by microscopy using special stains (Ziehl-Neelsen staining turns mycobacteria red against a blue background).
Most people encounter mycobacteria during their lifetime, yet far from everyone develops the disease: the state of the immune system plays a crucial role. When the pathogen enters the body, phagocytic cells attempt to engulf and digest the bacterium, but the mycobacterial cell wall is resistant to lysosomal enzymes. The phenomenon of incomplete phagocytosis develops: the pathogen survives inside the macrophage, which determines the chronic course of the infection.
Morphological Response of the Body
Unable to destroy the pathogen, the immune system confines it by forming a cellular wall around the focus. Morphologically, this manifests as the formation of a granuloma—a structure with caseous necrosis in the center, surrounded by epithelioid cells, lymphocytes, and Langhans giant cells.
Maintaining the granuloma requires constant energy and cellular resources. With preserved immune defenses, a primary complex and subsequently a Ghon focus (calcification) are formed. If immunity weakens, the barrier breaks down, leading to reactivation and progression of the infection. This explains the lifelong risk of relapse in infected individuals.
Risk Groups and Routes of Transmission
Particularly vulnerable are immunocompromised patients:
- HIV-infected individuals;
- people with primary and secondary immunodeficiencies;
- individuals not vaccinated with BCG in childhood;
- patients with protein-energy malnutrition;
- contacts of patients with active (open) tuberculosis.
Routes of transmission are diverse: airborne (primary), alimentary, contact, and transplacental. Consequently, tuberculosis can develop in virtually any organ except skin appendages: respiratory, intestinal, cutaneous, osteoarticular, urogenital, and other localizations are distinguished.
Clinical forms and diagnostics
There are numerous clinical forms of pulmonary tuberculosis: focal, infiltrative, disseminated, fibro-cavitary, cirrhotic, and others. The form determines treatment tactics and prognosis: focal usually has a favorable course, disseminated and infiltrative require prolonged therapy, and cirrhotic often requires surgical intervention.
The distinction between open and closed forms is of fundamental importance. Bacterial excretion is established exclusively by laboratory methods—sputum microscopy or culture—rather than by the presence of a cough. Contacts of patients with an open form are referred to a phthisiatrician, bypassing the general practitioner or pediatrician.
In children, symptoms are often subtle. Indications for evaluation include: prolonged cough with sputum unresponsive to broad-spectrum antibiotics, progressive weight loss, night sweats, low-grade fever, and contact with an infected person. Screening includes the Manttu test (Tuberculin skin test), Diaskintest, chest radiography or CT, sputum examination, and bronchoscopy with biopsy if necessary. A positive Manttu test does not equal disease: it may reflect post-vaccination immunity, and is therefore used as a guide for further investigation.
Treatment and Drug Resistance
Tuberculosis therapy is a prolonged, multi-drug chemotherapy regimen comparable in principle to cancer treatment. Combinations of drugs developed mainly in the mid-20th century are used, causing pronounced toxicity: hepatotoxicity, neurotoxicity, dyspeptic symptoms, headache, and depressive states.
The minimum course is rarely shorter than 6 months, and reaches 12–24 months for complicated forms. The key clinical problem is drug resistance. The initial pathogen population contains isolated resistant cells; premature discontinuation of medication causes sensitive strains to die, while resistant ones actively multiply, forming multidrug-resistant tuberculosis (MDR-TB). In Russia, up to 30% of newly diagnosed cases are MDR-TB, which significantly worsens the prognosis.
Supportive measures include a full, high-calorie diet, proper regimen, management of side effects with adjuvant drugs, and psychological support. Upon completion of the course, sanatorium-resort treatment and regular follow-up are indicated for the timely detection of reactivation.
Prevention
Specific prevention is based on BCG vaccination at the maternity hospital. The vaccine does not prevent infection, but protects against severe generalized forms—miliary tuberculosis and tuberculous meningitis, which are especially dangerous in childhood. An indirect sign of vaccination is the post-vaccination scar on the shoulder, although its absence does not rule out prior vaccination. Nonspecific prevention includes maintaining immunity, detecting and isolating bacterial excretors, and examining contacts.
Key points
- Tuberculosis is caused by Mycobacterium tuberculosis and runs a chronic course due to incomplete phagocytosis.
- The morphological substrate is a granuloma with caseous necrosis; the outcome of the primary focus is the Ghon focus.
- Main routes of transmission: airborne, alimentary, contact, transplacental.
- The disease develops predominantly in immunocompromised individuals and risk groups.
- Open and closed forms differ in bacterial excretion confirmed by laboratory tests.
- In children, symptoms are often sparse; screening includes the Manttu test, Diaskintest, and imaging.
- Treatment is prolonged and toxic; interrupting the course leads to multidrug resistance.
- The BCG vaccine protects not against infection, but against severe forms of tuberculosis in children.