Morphology and cellular composition of the infiltrate
Scleroma granuloma is a specific type of granulation tissue. The cellular infiltrate here has a strictly defined composition. The bulk consists of clusters of macrophages, T-lymphocytes, and plasma cells.
Particular attention is paid to plasma cells during microscopy. Specific eosinophilic inclusions—Russell bodies—are found in their cytoplasm. By nature, these bodies are antibody degradation products that accumulate inside the cell. The presence of Russell bodies serves as a crucial marker when studying the histological picture of scleroma.
Mikulicz cells and pathogenesis features
The triggering factor for granuloma development is the invasion of the pathogen—the Frisch-Volkowitsch bacillus. The pathogenesis of the disease is closely linked to the macrophage immune response.
First, macrophages engulf the bacilli and subject them to partial digestion. This is necessary to expose the antigenic determinants of the pathogen. During this interaction, macrophages undergo morphological transformation and turn into large Mikulicz cells. In pathological anatomy, these structures are considered a peculiar analogue of epithelioid cells.
The key feature of Mikulicz cells is that phagocytosis within them is incomplete. The bacilli do not die, but continue to persist inside the macrophage—a state of endocytobiosis develops.
Immune response and hypersensitivity development
The state of endocytobiosis cannot last forever. Sooner or later, the Mikulicz cells, overloaded with bacteria, rupture. At this moment, numerous viable pathogens are released into the surrounding tissues all at once.
Such a massive release of antigens leads to a sharp stimulation of the immune system. The reaction develops as delayed-type hypersensitivity (DTH). Despite such a vigorous cell-mediated immune response, effective protection is not formed: acquired immunity in scleroma is completely absent, allowing the process to progress for a long time.
Outcomes, complications, and life-threatening risks
Specific granulation tissue in scleroma has a marked tendency toward maturation. It transforms into dense coarse fibrous connective tissue. This process is called sclerosis.
The preferred localization of scleroma is the mucous membrane of the upper respiratory tract. The pathological process affects the nasal passages, larynx, trachea, and bronchi. Rapid sclerosis and tissue scarring inevitably cause stenosis (narrowing) of the airways. The clinical significance of this outcome is extremely high: the patient progressively develops worsening breathing difficulties, ultimately creating a risk of death from asphyxia.
Briefly: answers to topical questions
What is the macroscopic picture of the affected mucous membrane in scleroma?
Macroscopic changes in the mucous membrane of the upper respiratory tract in scleroma are characterized by rapid sclerosis. The proliferation of coarse fibrous connective tissue causes pronounced stenosis of the lumens of the nose, larynx, trachea, and bronchi. This deformation leads to clinically significant breathing difficulties and poses a direct threat of asphyxia.
What other specific granulomatous diseases must scleroma be differentiated from?
Scleroma must be differentiated from other infectious diseases characterized by the formation of specific chronic granulomas. These diseases include:
- Tuberculosis
- Syphilis
- Leprosy
- Glanders
These pathologies are grouped together as specific granulomas because their morphological picture clearly reflects the features of a particular disease. In contrast, non-specific granulomas lack characteristic etiological signs.
To memorize key facts, use the acronym S-M-A-R-T: S — Sclerosis (outcome into coarse fibrous tissue). M — Mikulicz cells (macrophages containing bacilli). A — Asphyxia (threat due to airway stenosis). R — Russell bodies (eosinophilic antibody degradation products). T — T-lymphocytes (part of the infiltrate).
Class and exam questions
What is the role of Russell bodies in scleroma granuloma?
Russell bodies are eosinophilic inclusions inside plasma cells. They form as a result of antibody degradation and are a characteristic component of the cellular infiltrate in scleroma.
What are Mikulicz cells and how do they form?
These are large transformed macrophages that act as an analogue of epithelioid cells. They form after normal macrophages engulf Frisch-Volkowitsch bacilli and partially digest them to reveal antigenic determinants.
Why is phagocytosis in scleroma considered incomplete?
Because the bacilli engulfed by macrophages are not completely destroyed. They remain viable inside Mikulicz cells, forming the phenomenon of endocytobiosis.
What is the main clinical danger of scleroma?
The disease affects the mucous membrane of the upper respiratory tract. Rapid maturation of granulation tissue into coarse fibrous connective tissue causes stenosis of the larynx, trachea, and bronchi, leading to breathing difficulties and the risk of asphyxia.
What else to study on this topic
- Mechanisms of delayed-type hypersensitivity (DTH) development upon the destruction of Mikulicz cells.
- The phenomenon of endocytobiosis: why macrophages are unable to complete the phagocytosis of Frisch-Volkowitsch bacilli.
- Comparative morphological characteristics of Mikulicz cells and classic epithelioid cells.
- Processes of antibody degradation and the formation of eosinophilic Russell bodies in plasma cells.
- Stages of maturation of specific granulation tissue into coarse fibrous connective tissue.
- Pathophysiology of airway stenosis and the development of asphyxia during sclerosis.
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