Morphology and Cell Wall
Tuberculosis agents belong to the family Mycobacteriaceae. They are Gram-positive, non-motile, non-spore-forming rods prone to pronounced polymorphism (e.g., M. tuberculosis are long and slender, whereas M. bovis are short and thick).
Their critical feature is a complex cell wall rich in lipids (up to 40% of dry weight), containing mycolic acid, peptidoglycan, and lipoarabinomannan. Because of this "waxy armor," the bacteria poorly absorb standard aniline dyes. Ziehl–Neelsen staining is used to identify them, confirming their acid-fast properties. Under adverse conditions, the pathogen can transition into L-forms, ensuring long-term persistence.
Cultural and Biochemical Properties
Mycobacteria are extremely fastidious and grow very slowly. Rich media (Löwenstein–Jensen, Petragnani) are used for cultivation, supplemented with growth stimulators (lecithin, vitamins) and substances that neutralize their own toxic metabolites (albumin, charcoal).
- M. tuberculosis is an obligate aerobe. On liquid media, it forms a wrinkled pellicle in 5–7 days, and on solid media, it produces dry, cauliflower-like R-form colonies.
- M. bovis is a microaerophile, grows even slower, and forms smooth S-form colonies.
Biochemically, the agents exhibit high catalase activity. The human species synthesizes large amounts of niacin (positive Konno test) and reduces nitrates to nitrites, which helps differentiate it from the bovine species.
Pathogenesis Factors and Immunity
Mycobacteria do not secrete classical exotoxins. Their pathogenicity stems from their ability to survive and replicate inside pulmonary macrophages.
Defense mechanisms against phagocytosis include the synthesis of sulfolipids and cord factor (trehalose 6,6'-dimycolate), which together block phagosome-lysosome fusion. Additionally, bacteria produce ammonia to alkalinize the environment and neutralize oxygen radicals. Tissue destruction in tuberculosis is largely linked not to the bacteria themselves, but to the immune system's response—delayed-type hypersensitivity (Type IV), which leads to granuloma formation and caseous necrosis.
Epidemiology and Resistance
The primary source of infection is an individual with pulmonary tuberculosis, and the main transmission route is aerogenic (airborne droplet and dust).
Due to their lipid cell wall, the pathogen is extremely resistant in the environment, withstanding drying and many disinfectants (requiring activated solutions with exposures of several hours). However, bacteria are rapidly killed by UV radiation (in 2–3 minutes) and boiling (in 5 minutes). Disease develops in only about 10% of infected individuals; in the rest, the process is contained by the formation of an asymptomatic Ghon focus.
Laboratory Diagnostics
A combination of methods is used to detect the pathogen:
- Bacterioscopy: Ziehl–Neelsen staining of sputum smears or fluorescence microscopy (detects mycobacteria even in small quantities, sometimes using concentration techniques like flotation).
- Bacteriological culture: The "gold standard" with extremely high sensitivity. Due to slow growth, classical culture takes 3–6 weeks; therefore, automated systems (such as BACTEC) are now widely used to shorten turnaround time.
- Molecular genetic methods (PCR): Provide rapid results and are used alongside microscopy for rapid diagnostics.
- Tuberculin skin testing: The Mantoux test and Diaskintest are used to detect infection status (specific sensitization), particularly in children.