Entry and Primary Replication of the Pathogen
Infection occurs by rubbing infected body louse feces into skin scratch marks (the minimal dose is only 10 rickettsiae). Rickettsiae penetrate into endotheliocytes of lymphatic and blood capillaries at the site of entry. Inside cells, they actively multiply, forming so-called Moser cells—hypertrophied endotheliocytes containing up to a thousand bacteria.
Using the enzyme phospholipase A2, rickettsiae destroy the membrane of the affected cell. By approximately the 5th–7th day of the incubation period, these cells die and desquamate, releasing pathogens into the bloodstream—this is the first wave of rickettsiemia.
Generalization of Infection and Vascular Damage
Once in the blood, rickettsiae are carried throughout the body and invade the endothelium of the microvasculature (capillaries, precapillaries, venules, arterioles), forming multiple secondary foci. Specific inflammation of the vessel wall develops—proliferative-desquamative vasculitis (endovasculitis, panvasculitis, perivasculitis).
Endothelial injury triggers a cascade of pathological reactions:
- The edges of the damaged vessel are covered with platelets and leukocytes, forming parietal coagulation thrombi (endothrombovasculitis).
- A massive release of eicosanoids and other inflammatory mediators occurs, leading to arterial hypotension and increasing intoxication.
- Microcirculation is disrupted: paralytic hyperemia, slowed blood flow, and stasis occur.
- Vascular wall permeability increases, the liquid part of the blood escapes into tissues (plasmarrhagia), reducing the circulating blood volume.
As a result of these processes, hypoxemia, tissue hypoxia, and metabolic acidosis develop.
Peak Period and Formation of Specific Granulomas
During the peak period of the disease (after the appearance of the rash), rickettsiemia is sustained by the continuous release of bacteria from newly destroyed endotheliocytes. The level of inflammatory mediators in the blood reaches its maximum, clinically manifested by the peak of the intoxication syndrome.
Generalized vascular damage is especially pronounced in the brain and its membranes, as well as in the skin and myocardium. Macrophages and mononuclear cells accumulate around the necrotic areas of the vessel wall, forming specific typhus nodules (Popov granulomas). In parallel, phagocytosis of pathogens is triggered, and the production of specific antibodies begins, which ultimately leads to clinical recovery, though immunity remains non-sterile (rickettsiae persist in the body).
Briefly: answers to topical questions
What is the name of the relapse of epidemic typhus that occurs years later due to non-sterile immunity?
The relapse of epidemic typhus occurring years later due to non-sterile immunity is called Brill-Zinsser disease.
This disease represents an endogenous relapse of infection occurring in the absence of an external source and pediculosis. The pathogenetic basis is the long-term persistence of rickettsiae in the endotheliocytes of the circulatory and lymphatic systems of a previously infected person. With the development of immunosuppression of any origin, the infection is activated, leading to the manifestation of relapse many years or decades after the primary disease.
What morphological elements represent the exanthem in epidemic typhus?
The exanthem in epidemic typhus has a roseolous-petechial character. Morphological elements:
- roseolae: do not rise above the skin, have scalloped edges, disappear upon pressure; persist for 4–5 days and disappear without a trace;
- primary petechiae: appear simultaneously with roseolae;
- secondary petechiae: may appear over time in the center of roseolae.
Petechiae disappear in 10–13 days, gradually fading and changing color. The rash elements are described as bright, abundant, 1–3 mm in diameter, on a hyperemic background.
What pathomorphological changes occur in the myocardium in severe typhus?
In typhus, myocardial findings in the sources indicate:
- acute interstitial myocarditis;
- vasculitis at sites of rickettsial multiplication, predominantly in the microvasculature;
- in destructive thrombovasculitis, complete obliteration of part of the microvasculature followed by vascular destruction;
- formation of specific typhus granulomas around damaged vessels; the myocardium is among the target organs with the highest accumulation of granulomas.
What neurological complications develop in typhus meningoencephalitis?
In typhus meningoencephalitis, meningeal symptom complexes are combined with focal symptoms. Indicated neurological manifestations:
- limb tremor;
- generalized tremor;
- seizure disorder;
- swallowing disorders;
- dysarthria;
- coma vigile—complete immobility of the patient with preserved consciousness; the outcome of this condition is generally death.
Class and exam questions
What is a Moser cell?
This is a hypertrophied endothelial cell (target cell) inside which *Rickettsia prowazekii* has multiplied (containing up to 1000 bacteria). Its destruction leads to the release of rickettsiae into the bloodstream.
Why does blood pressure drop in typhus?
Hypotension occurs due to a massive release of inflammatory mediators (eicosanoids) upon the death of endotheliocytes, paralytic vascular hyperemia, and a decrease in circulating blood volume due to plasmarrhagia.
What is the main mechanism of infection?
Infection occurs via contact: the person rubs infected body louse feces into scratch marks from bites (percutaneous infection).
What else to study on this topic
- Forms of existence of *Rickettsia prowazekii* (vegetative, filterable, resting)
- Antigenic structure of *Rickettsia prowazekii*
- Brill-Zinsser disease (recrudescence typhus)
- The role of the louse as a vector and the "5-Day Rule"
- Clinical features and diagnosis of epidemic typhus
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