Primary Tuberculosis Complex
Primary tuberculosis develops upon the body's first encounter with the mycobacterium. Its morphological substrate is the primary tuberculosis complex, consisting of three components: the primary affect in the lung, lymphangitis, and regional caseous lymphadenitis.
The further fate of the complex varies. In a favorable course, the process subsides: the primary affect undergoes scarring and petrification, forming a Ghon focus, and when the lymph node also heals, it is referred to as a Ghon complex — a petrificate with fibrosis along the course of the lymphangitis.
Progression of Primary Tuberculosis
If resolution does not occur, several pathways of progression are possible.
- Enlargement of the primary affect with expansion of the zone of caseous necrosis and the development of caseous pneumonia, followed by the formation of a pulmonary cavity (predominantly in the upper lobes of the lungs).
- Hematogenous generalization—spread of the pathogen into the bloodstream and dissemination to various organs. It can be miliarly (small seed-like disseminations) or macronodular.
- Basilar leptomeningitis—dissemination into the meninges.
- Lymphogenous generalization with spread along lymphatic pathways.
Symmetrical apical seedings in the lungs during hematogenous dissemination are called Simon foci; they serve as the substrate for subsequent secondary tuberculosis.
Hematogenous Tuberculosis
Develops against the background of a healed primary complex while dormant infection persists. Three groups of forms are distinguished.
- Generalized hematogenous tuberculosis: hyperacute tuberculous sepsis, acute generalized miliary, and acute generalized macronodular tuberculosis.
- With predominantly pulmonary manifestations: miliary pulmonary tuberculosis—lungs are sprinkled with small tubercles and hyperinflated due to emphysema; macronodular variant.
- With predominantly extrapulmonary manifestations: osteoarticular form (tuberculous spondylitis with destruction of vertebral bodies and intervertebral discs, formation of cold abscesses and gibbus), urogenital (tuberculosis of the Fallopian tubes with risk of ectopic pregnancy), cutaneous, and tuberculous meningitis.
Tuberculous Granuloma
The microscopic basis of all forms is the tuberculous granuloma. In the center lies caseous necrosis, surrounded by a palisade of epithelioid cells. Diagnostically significant are Langhans giant multinucleated cells with a horseshoe-shaped arrangement of nuclei. A lymphocytic infiltrate is located at the periphery. An important feature: blood vessels are absent within the granuloma.
Secondary Tuberculosis: Eight Phases
Secondary tuberculosis develops decades after primary infection during a sharp decline in immunity. The lungs are predominantly affected without involvement of regional lymph nodes; spread occurs by contact and intracanalicularly via the bronchi. Eight sequential clinical and morphological form-stages are distinguished.
- Acute focal tuberculosis—formation of the Abrikosov focus in areas of reinfection, most often at the site of old Simon foci.
- Fibro-focal tuberculosis—scarring and encapsulation of the Abrikosov focus resulting in the formation of Aschoff–Puhl foci.
- Infiltrative tuberculosis—appearance around old foci of caseous necrosis mixed with an exudative-cellular infiltrate—Assmann–Redeker foci, which are visible radiologically.
- Tuberculoma — an encapsulated focus with a thin capsule prone to rupture.
- Caseous pneumonia — massive necrosis of lung tissue accompanied by fibrinous pleurisy.
- Acute cavernous tuberculosis — rapid formation of a cavity communicating with a bronchus; dangerous due to bronchogenic dissemination and shedding of mycobacteria during coughing (pulmonary consumption).
- Fibro-cavernous tuberculosis — chronic progression with a fibrous cavity wall. A characteristic feature is the "tier-like" arrangement of lesions: old foci lie above the cavity, fresher ones below; extension to the contralateral lung is typical.
- Cirrhotic tuberculosis — massive proliferation of connective tissue, diffuse pulmonary sclerosis, and lung deformation with adhesions and bronchiectasis.
Complications and outcomes
Prognosis is determined not by the inflammation itself, but by its complications.
- Hemorrhage from the cavity leading to post-hemorrhagic anemia and death.
- Rupture of the cavity into the pleural cavity, resulting in pneumothorax and pleural empyema.
- Secondary amyloidosis resulting in chronic kidney disease.
- Bronchogenic dissemination complicated by bronchial tuberculosis.
Key points
- The primary tuberculosis complex includes the primary affect, lymphangitis, and caseous lymphadenitis; healing leads to the formation of the Ghon focus (complex).
- Symmetrical apical disseminations in hematogenous generalization are called Simon foci.
- Hematogenous tuberculosis is divided into generalized, predominantly pulmonary, and predominantly extrapulmonary forms.
- The morphological basis of all forms is a granuloma with caseous necrosis and Langhans cells, devoid of blood vessels.
- Secondary tuberculosis begins with the Abrikosov focus and goes through eight stages up to the cirrhotic form.
- Aschoff–Puhl foci correspond to the fibro-focal form, and Assmann–Redeker foci correspond to the infiltrative form.
- Fibro-cavernous tuberculosis is characterized by a tier-like structure: older lesions are located above, and fresher ones below the cavity.
- The main causes of death are pulmonary hemorrhage, pneumothorax with empyema, and amyloidosis complicated by chronic kidney disease.