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Pathological Anatomy · Inflammation

Granulomatous inflammation

Inflammatio granulomatosa

Granulomatous inflammation is a specific type of inflammatory process characterized by the formation of localized nodules (granulomas) in tissues. The basis of their formation is the active proliferation and morphological transformation of phagocytic cells. This type of tissue reaction aims to localize pathogenic agents, and its outcomes depend on the affected organ and the nature of the pathogen.

Nodule sizeThe diameter of granulomas usually does not exceed 1–2 mm, and they are predominantly detected under a microscope.
Epidemic typhusAffects the gray matter of the CNS and peripheral nervous system, resulting in glial scar formation.
Typhoid feverGranulomas form in the solitary follicles of the small intestine from reticular cells.
Intestinal outcomeUpon recovery from typhoid fever, complete restitution of the intestinal wall occurs without a trace.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Morphological features of granulomas

Granulomas are compact, well-demarcated clusters of cells that arise in response to tissue damage. Their physical size is typically extremely small: the diameter of a typical nodule usually does not exceed 1–2 mm. Because of such microscopic dimensions, they are rarely detected macroscopically (with the naked eye), so their detailed study and verification of cellular composition require mandatory microscopic examination of histological preparations.

Typhus granulomas in the nervous system

In epidemic typhus, the pathological process selectively affects the structures of the central and peripheral nervous system. The formation of specific nodules is based on small-focal necrosis of groups of neurons or ganglion cells. These changes are predominantly localized in the gray matter of the brain or spinal cord.

The cellular composition of an already formed typhus granuloma is quite diverse. It includes dense clusters of macrophages, lymphocytes, pericytes, as well as isolated neutrophils. An important morphological feature is that in the center of a mature nodule, the blood vessel that initiated the lesion is destroyed and is no longer identifiable.

In response to nerve tissue damage, a pronounced glial defense reaction occurs. Foci of necrotic tissue are densely surrounded by glial elements, which assume the function of macrophage-phagocytes. The outcome of this process is the gradual resorption (clearance) of dead masses by glial cells and the formation of persistent glial scars in their place.

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Brain involvement in rabies and neuroinfections

In rabies and a number of other neuroinfections, the triggering mechanism of inflammation is direct damage to the walls of microcirculatory blood vessels. This is provoked by the direct action of infectious agents or their secreted toxins. As a result of circulatory disorders 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 such lesions is quite characteristic. Dense lymphoid and monocytic infiltrates form around hyperemic (congested) capillaries and venules. Nerve cells located in the immediate vicinity of damaged vessels undergo severe dystrophy and subsequent necrosis. Active proliferation of microglia cells is observed around the dead neurons.

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

Typhoid granulomas in the intestine

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

Morphologically, such nodules are clusters of active phagocytes that have transformed from local reticular cells. In pathological anatomy, these modified elements are called "typhoid" cells. They are distinguished by their large size, regular round shape, and characteristic light cytoplasm. Their main biological task is to intensively phagocytose S. typhi bacteria, as well as to absorb the resulting cellular detritus.

The dynamics of typhoid granuloma development are strictly regular and include several sequential stages:

  1. Formation of the cell nodule.
  2. The stage of necrosis in typhoid granulomas. Tissue death is directly related to the damaging effect of Salmonella endotoxins, which were phagocytosed but not destroyed by phagocytes.
  3. Outcome. In the case of a favorable course of the disease and patient recovery, acute granulomas disappear without a trace. The process ends with complete restitution—absolute restoration of the normal structure of the intestinal wall without scar formation.

Briefly: answers to topical questions

What types of cells underlie granulomatous inflammation, and what does its outcome depend on?

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

The cellular composition of granulomas may include:

  • macrophages and monocytic phagocytes;
  • epithelioid cells;
  • giant cells, including Pirogov-Langhans cells or foreign body giant cells;
  • lymphocytes, pericytes, isolated neutrophils;
  • in non-immune granulomas—a small number of leukocytes, including eosinophils.

Non-immune granulomas typically lack epithelioid cells.

The outcome depends on the immune status of the organism: granuloma resorption, scarring, or progression with generalization of the process are possible. In lesions of the nervous system, the clinical outcome depends on the localization and volume of scarring.

How to memorize

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

Class and exam questions

What is the size of a typical granuloma?

The diameter of the nodules is usually 1–2 mm. Because of this small size, microscopic examination is required for their detection and detailed study.

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

These are large, rounded macrophages with light cytoplasm, formed from reticular cells. They form specific granulomas in the lymphoid follicles of the small intestine in 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 in nervous tissue end?

Dead neurons and foci of necrosis are phagocytosed by glial cells. As an outcome of the process, persistent glial scars form at the site of the destroyed nerve tissue.

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What else to study on this topic

  • Cellular composition of the typhus granuloma: the role of pericytes, macrophages, and lymphocytes
  • Mechanisms of microcirculatory damage in neuroinfections and rabies
  • Dynamics of granuloma formation and necrosis in solitary follicles in typhoid fever
  • Differences between focal necroses of the gray and white matter of the brain
  • The process of transformation of reticular cells into macrophages with light cytoplasm

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