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Scleroma Granuloma

Scleroma

For medical students2 min readUpdated 2026-10-10

Scleroma is a specific type of granulation tissue that develops in the mucous membrane of the upper respiratory tract in response to infection by Klebsiella rhinoscleromatis (Frisch bacilli). Its primary clinical danger lies in the aggressive proliferation of dense fibrous connective tissue, leading to narrowing of the airways and the risk of asphyxia.

Causative agentFrisch bacillus (*Klebsiella rhinoscleromatis*)

Marker cellsMikulicz cells and Russell bodies

LocalizationMucous membrane of the upper respiratory tract

Main threatAirway stenosis and development of asphyxia

Morphology and Cellular Composition of the Infiltrate

Scleroma granuloma is a unique form of granulation tissue. The cellular infiltrate has a strictly defined composition, primarily consisting of macrophages, T lymphocytes, and plasma cells.

Microscopy reveals a notable focus on plasma cells. Their cytoplasm contains specific eosinophilic inclusions known as Russell bodies. Structurally, these bodies represent aggregated products of antibody degradation accumulating intracellularly. The presence of Russell bodies serves as a vital marker when studying the histological picture of scleroma.

Mikulicz Cells and Pathogenesis

The triggering factor for granuloma development is infection by the Frisch bacillus. The pathogenesis of the disease is closely tied to the macrophage-mediated immune response.

Initially, macrophages engulf the bacilli and partially digest them to process and present antigenic determinants. During this interaction, macrophages undergo morphological transformation into large Mikulicz cells. In pathology, these structures are regarded as a specific analogue of epithelioid cells.

A key feature of Mikulicz cells is that phagocytosis is incomplete. The bacilli are not destroyed and continue to survive inside the macrophage, establishing a state of endocytobiosis.

Immune Response and Hypersensitivity

Endocytobiosis cannot persist indefinitely. Sooner or later, Mikulicz cells engorged with bacteria rupture. At this moment, numerous viable pathogens are suddenly released into the surrounding tissue.

This massive release of antigens triggers a pronounced cell-mediated immune reaction via a type IV delayed-type hypersensitivity (DTH) mechanism. Despite this vigorous cellular immune response, effective protection is not established; acquired immunity in scleroma is essentially absent, allowing the pathological process to progress chronically.

Outcomes, Complications, and Life-Threatening Risks

The specific granulation tissue in scleroma has a strong tendency toward maturation, eventually transforming into dense, coarse fibrous connective tissue. This process is termed sclerosis.

The preferred site of involvement is the upper respiratory tract mucosa, affecting the nasal passages, larynx, trachea, and bronchi. Aggressive sclerosis and tissue scarring inevitably cause stenosis (narrowing) of the respiratory lumen. The clinical consequence of this outcome is profound: progressive respiratory distress that ultimately creates a life-threatening risk of asphyxia.

Mnemonic

To memorize key facts, use the acronym S-M-A-R-T: S — Sclerosis (progression to 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).

Frequently asked questions

What is the gross (macroscopic) appearance of the affected mucosa in scleroma?

Macroscopic changes in the upper respiratory tract mucosa in scleroma are characterized by extensive sclerosis. The proliferation of coarse fibrous connective tissue causes marked stenosis of the lumina of the nose, larynx, trachea, and bronchi. This deformation leads to clinically significant respiratory impairment 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 include:

Tuberculosis
Syphilis
Leprosy
Glanders

These pathologies are grouped as specific granulomas because their morphological picture clearly reflects the features of the causative agent. In contrast, non-specific granulomas lack such characteristic etiologic markers.

What is the role of Russell bodies in scleroma granuloma?

Russell bodies are eosinophilic inclusions within plasma cells. They form as a result of antibody degradation and serve as a characteristic component of the cellular infiltrate in scleroma.

What are Mikulicz cells and how do they form?

They are large transformed macrophages that act as analogs of epithelioid cells. They form after regular macrophages phagocytose Frisch bacilli and partially digest them to expose 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, establishing the phenomenon of endocytobiosis.

What is the primary clinical danger of scleroma?

The disease affects the mucous membrane of the upper respiratory tract. The aggressive maturation of granulation tissue into coarse fibrous connective tissue causes stenosis of the larynx, trachea, and bronchi, leading to respiratory failure and the threat of asphyxia.

Go deeper

Mechanisms of delayed-type hypersensitivity (DTH) upon the destruction of Mikulicz cells.
The phenomenon of endocytobiosis: why macrophages fail to complete the phagocytosis of Frisch 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 tissue sclerosis.