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Pathological Anatomy · Chapter 16. Infectious and Parasitic Diseases

Rickettsiosis

Rickettsioses

Rickettsial infections are a group of acute infectious diseases caused by intracellular bacteria. The main target of the pathogen in the body is the endothelium of small blood vessels, the destruction of which leads to generalized vasculitis, thrombosis, and severe intoxication.

Main targetEndothelium of microcirculatory vessels
Cause of deathAcute heart failure (most common)
Dangerous complicationDisseminated intravascular coagulation (DIC) due to activation of the blood clotting system
Specific markerPopov's typhus granulomas (nodular infiltrates)
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

Classification of rickettsial infections

In human pathology, three diseases have the greatest epidemiological and clinical significance: epidemic typhus, endemic typhus, and Q fever.

In addition to these, the classification includes:

  • Rocky Mountain spotted fever;
  • Mediterranean spotted fever (caused by R. conorii);
  • Tick-borne typhus and North Queensland tick typhus;
  • Rickettsialpox;
  • Tsutsugamushi fever and trench fever;
  • Tick-borne paroxysmal rickettsiosis (trench fever).

General pathogenesis of vascular disorders

At the cellular level, rickettsiae bind to cholesterol-containing receptors and enter endothelial cells via endocytosis. Intracellular reproduction of the pathogen inevitably leads to the destruction of endothelial cells.

This process triggers a cascade of severe vascular changes:

  1. Segmental or circular fibrinoid necrosis develops in the vessel wall, accompanied by perivascular granulomatous inflammation.
  2. Release of endotoxin activates the kallikrein-kinin system, causing local blood coagulation.
  3. Disseminated vascular thrombosis develops. Ischemia and necrosis of perivascular tissues clinically manifest as a characteristic maculopapular rash.
  4. Vascular permeability increases, leading to edema and hemorrhages. Activation of the coagulation system often leads to DIC.

Generalized damage to the microvasculature causes meningoencephalitis, depression of the vasomotor center, sympathetic nervous system, and adrenal glands. This leads to a sharp drop in blood pressure and respiratory failure.

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Epidemic typhus and its morphology

This is a particularly dangerous infection caused by Rickettsia prowazekii (Rickettsia prowazekii). The source of infection is a sick person, and the vector is the body louse or (less commonly) the head louse.

The macroscopic picture lacks strict specificity: a reddish-brown rash is noted, along with dull and edematous meninges, a plethoric brain, an enlarged spleen, and fatty degeneration of parenchymal organs.

The main morphological substrate of the disease is generalized typhus vasculitis, which develops in four stages:

  1. Swelling, destruction, and desquamation of the endothelium (destructive endovasculitis).
  2. Thrombus formation in capillaries and arterioles at the sites of injury (destructive endotrombovasculitis).
  3. Proliferation of endothelium and pericytes (destructive-proliferative endotrombovasculitis).
  4. Formation of lymphoid infiltrates in the vessel walls.

The most typical histological sign is Popov's typhus granulomas. These are nodular foci of endo- and perivascular infiltration that abundantly form in the brain (especially in the medulla oblongata), myocardium, and endocrine glands.

Rocky Mountain spotted fever and Q fever

  • Rocky Mountain spotted fever: Transmitted by ixodid ticks. A primary affect in the form of an eschar forms at the bite site. After the pathogen enters the blood, generalized vasculitis with fibrinoid necrosis develops. Thrombosis of large cerebral arterioles can lead to demyelination of nervous tissue and cerebral infarctions. Pneumonitis may also develop.
  • Q fever (Central Asian fever): Caused by coxiellae (Coxiella). Like other rickettsial infections, it affects the microvasculature. However, it is characterized by the formation of perivascular macrophage granulomas in the liver, spleen, bone marrow, and brain, as well as the development of interstitial pneumonia, which morphologically closely resembles viral pneumonia.

Briefly: answers to topical questions

Which complications of epidemic typhus most often lead to a fatal outcome?

Fatal outcome in epidemic typhus results from acute heart failure, as well as complications involving the central nervous system and blood vessels.

  • Acute heart failure is the most frequent cause of death.
  • Central nervous system involvement is a rarer cause of death.
  • Vascular complications are also listed among the causes of unfavorable prognosis and death.

What is the histological structure of the primary affect in Rocky Mountain spotted fever?

In Rocky Mountain spotted fever, a small eschar forms at the tick bite site, representing the primary affect. The exact histological structure of the primary affect itself is not detailed in the sources.

The following microscopic changes are noted for the rash elements:

  • Microcirculatory vessels — fibrinoid necrosis of the walls.
  • Perivascular zone — granulomatous inflammation with fibrin deposition and necrosis development.

Which insects and animals are vectors and reservoirs of endemic typhus?

Endemic (murine) typhus is an acute zoonotic disease. Various rodents serve as the natural reservoir, and their ectoparasites act as vectors.

  • Reservoir — rodents (rats, house mice), opossums, cats.
  • Vectors — animal ectoparasites (tropical fleas, cat fleas, and rodent fleas).

What are the features of morphological changes in the myocardium in epidemic typhus?

Morphological changes in the heart in epidemic typhus are characterized by the development of a specific inflammatory process in the interstitial tissue of the myocardium. The stroma of the heart muscle is involved in the pathological process.

  • Acute interstitial myocarditis — focal infiltration of the stroma by lymphocytes, plasmacytes, and formation of granulomas.
  • Diffuse involvement — inflammation is less commonly diffuse in nature.
How to memorize

To memorize the organs where Popov's typhus granulomas NEVER occur, use the acronym PLBM: Liver (Pechen), Spleen (Selezenka), Lymph nodes (Limfuzly), Bone marrow (Kostny mozg).

Class and exam questions

How exactly does a person contract epidemic typhus?

The pathogen is not transmitted directly via saliva during a louse bite. A person becomes infected when they scratch the itchy bite site and actively rub the feces of the infected insect into skin microtraumas.

What is Brill-Zinsser disease?

This is an endogenous relapse of epidemic typhus. Rickettsiae are capable of persisting in the body of a recovered person for decades and causing a recurrent disease (in a milder form) when immunity decreases.

What specific symptoms are visible upon external examination of a patient with typhus?

Rosenberg's enanthema (petechiae on the soft palate mucosa), "rabbit eyes" syndrome (scleral vessel injection), and Chiari-Avtsyn spots (purplish-bluish spots on the conjunctiva) are characteristic.

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What else to study on this topic

  • Nervous system involvement in rickettsial infections: meningoencephalitis and sympathetic ganglionitis
  • Complications of typhus: persistent hypotension, trophic disorders, and secondary infections
  • Lyme disease: stages of development, targets, and mechanism of cross-reactive autoimmunity
  • Joint pathomorphology in chronic Lyme disease (formation of "onion-skin structures")
  • HIV infection and AIDS: etiology, risk groups, and development of opportunistic infections

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