Sechenov School
Home › Pathology › Granulomatous Inflammation

Granulomatous Inflammation

Inflammatio granulomatosa

For medical students2 min readUpdated 2026-10-10

Granulomatous inflammation is a specific type of inflammatory response characterized by the formation of localized nodules (granulomas) in tissues. Their formation is driven by the active proliferation and morphological transformation of phagocytic cells. This tissue reaction aims to localize pathogens, and its outcomes depend on the affected organ and the nature of the causative agent.

Nodule SizeThe diameter of granulomas typically does not exceed 1–2 mm; they are primarily identified microscopically.
Epidemic TyphusAffects the gray matter of the central and peripheral nervous systems, resolving in glial scar formation.
Typhoid FeverGranulomas form in the solitary follicles of the small intestine from reticular cells.
Intestinal OutcomeRecovery from typhoid fever involves complete restitution of the intestinal wall without a trace.

Morphological Features of Granulomas

Granulomas are compact, well-demarcated collections of cells that arise in response to tissue injury. Their physical size is generally extremely small: the diameter of a typical nodule rarely exceeds 1–2 mm. Because of these microscopic dimensions, they are rarely identified macroscopically (with the naked eye). Therefore, detailed study and verification of their cellular composition require mandatory microscopic examination of histological preparations.

Epidemic Typhus Granulomas in the Nervous System

In epidemic typhus, the pathological process selectively affects structures of the central and peripheral nervous systems. Specific nodules form around microfocal necroses of neuron groups or ganglion cells. These changes predominantly localize in the gray matter of the brain or spinal cord.

The cellular composition of a mature epidemic typhus granuloma is quite diverse. It includes dense accumulations of macrophages, lymphocytes, pericytes, and occasional neutrophils. An important morphological feature is that in the center of a mature nodule, the blood vessel that initiated the injury is destroyed and is no longer identifiable.

In response to neural tissue damage, a prominent glial defense reaction occurs. Foci of necrotic tissue are densely surrounded by glial elements that assume the function of phagocytic macrophages. The ultimate outcome of this process is the gradual resorption (clearance) of dead cell masses by glial cells and the formation of permanent glial scars in their place.

Brain Involvement in Rabies and Neuroinfections

In rabies and several other neuroinfections, the initiating mechanism of inflammation is direct damage to the microvasculature walls. This is provoked by the direct action of infectious agents or their secreted toxins. As a result of circulatory disturbances and toxic effects, focal necroses develop in the tissues, which, unlike epidemic typhus, affect both the gray and white matter of the brain.

The microscopic picture of these lesions is quite characteristic. Dense lymphoid and monocytic infiltrates form around hyperemic (congested) capillaries and venules. Nerve cells located in close proximity to damaged vessels undergo severe dystrophy followed by necrosis. Active proliferation of microglial cells is observed around the dead neurons.

As with epidemic typhus, the inflammatory process culminates in the formation of glial scars (nodules). The subsequent clinical outcome for the patient directly depends on the functional areas of the brain where scarring occurred and the overall volume of damaged tissue.

Typhoid Granulomas in the Intestine

Typhoid fever is accompanied by the development of specific granulomas in the lymphoid structures of the digestive tract. The favored localization of this process is the solitary follicles of the small intestine.

Morphologically, these nodules represent clusters of active phagocytes transformed from local reticular cells. In pathological anatomy, these modified elements are termed typhoid cells. They are characterized by large sizes, regular round shapes, and distinct pale cytoplasm. Their primary biological function is to intensely phagocytose S. typhi bacteria and absorb cellular debris.

The developmental dynamics of the typhoid granuloma are strictly patterned and include several sequential stages:

  1. Formation of the cellular nodule.
  2. Stage of necrosis of the typhoid granulomas. Tissue death is directly linked to the lethal action of Salmonella endotoxins that were phagocytosed but not destroyed by the phagocytes.
  3. Outcome. In favorable cases of the disease and patient recovery, acute granulomas disappear without a trace. The process ends with complete restitution—the absolute restoration of the normal structure of the intestinal wall without scar formation.

Mnemonic

To easily remember inflammation outcomes, focus on the tissue: in the nervous system (epidemic typhus, rabies), dead neurons do not regenerate—a glial scar always forms. Conversely, in the mucosa of the small intestine (typhoid fever), recovery leads to complete restitution, meaning the granulomas vanish without a trace.

Frequently asked questions

What types of cells underlie granulomatous inflammation, and what determines its outcome?

Granulomatous inflammation is based on the proliferation and transformation of phagocytes with granuloma formation.

The cellular composition of granulomas may include:

  • Macrophages and monocytic phagocytes;
  • Epithelioid cells;
  • Giant cells, including Langhans giant cells or foreign body giant cells;
  • Lymphocytes, pericytes, occasional neutrophils;
  • In non-immune granulomas—a minimal number of leukocytes, including eosinophils.

Epithelioid cells are typically absent in non-immune granulomas.

The outcome depends on the immune status of the organism: resorption of the granuloma, fibrosis/scarring, or progression with generalization of the process. In central nervous system involvement, the clinical outcome depends on the localization and volume of scarring.

What is the size of a typical granuloma?

The diameter of the nodules is usually 1–2 mm. Due to such small dimensions, microscopic examination is required for their detection and detailed study.

What are 'typhoid cells' and where are they found?

These are large, round macrophages with pale cytoplasm that develop from reticular cells. They form specific granulomas in the lymphoid follicles of the small intestine during typhoid fever.

Why do typhoid granulomas undergo necrosis?

Necrosis occurs due to the damaging action of Salmonella toxins (S. typhi). These bacteria are phagocytosed by typhoid cells, after which their toxins destroy the granuloma itself.

How does granulomatous inflammation end in neural tissue?

Dead neurons and foci of necrosis are phagocytosed by glial cells. As a result, permanent glial scars form at the site of the destroyed neural tissue.

Go deeper

More topics in Pathology

Productive InflammationAortic Valve DiseasePneumoconioses and SilicosisCholangiocarcinomaAcute Lymphoblastic LeukemiaTumor-Host InteractionHeart Transplantation: Pathology, Rejection, and ComplicationsMyeloma KidneyGastritis: Acute and Chronic Forms, OLGA SystemHepatoblastoma and Vascular Liver TumorsMalariaChronic Lymphocytic LeukemiaPathology →