Typhus - What's going on?

Pathogenesis of epidemic typhus

The gateway for infection is minor skin lesions (usually scratches). Within 5-15 minutes, rickettsiae enter the bloodstream, where some of them die under the influence of bactericidal factors. And the bulk of the pathogens penetrate the vascular endothelium. In the cytoplasm of these cells, rickettsiae actively reproduce, which causes swelling, destruction and desquamation of the endothelium with the development of rickettsiemia. In the blood, some rickettsiae die, releasing endotoxin, while other microorganisms penetrate into the still undamaged cells of the endothelium of small vessels of various organs. This cycle is repeated without visible clinical manifestations until a sufficient amount of rickettsiae and their toxins accumulates in the body, which will lead to corresponding functional and organic changes in the vessels, organs and tissues. This process corresponds to the incubation period and the first 2 days of the febrile period.

The rickettsial endotoxin (LPS complex) circulating in the blood has a vasodilating effect in the system of small vessels - capillaries, precapillaries, arterioles, venules, causing a disruption of microcirculation, up to the formation of paralytic hyperemia with a slowdown in blood flow, a decrease in diastolic blood pressure, the development of tissue toxic hypoxia and the possible formation of DIC syndrome.

Pathomorphology of epidemic typhus

When rickettsia multiplies and endothelial cells die, specific typhus granulomas are formed.

The pathomorphological basis of typhus is generalized destructive-proliferative endovasculitis, which includes three components:

• thrombus formation;
• destruction of the vascular wall;
• cell proliferation.

Around the affected vessels in all organs and tissues, except for the liver, bone marrow and lymph nodes, focal cellular proliferation, accumulation of polymorphic cellular elements and macrophages with the formation of specific typhus granulomas, called Popov-Davydovsky nodules, occurs. Most of them are in the skin, adrenal glands, myocardium and, especially, in the vessels, membranes and substance of the brain. In the central nervous system, lesions are observed mainly in the gray matter of the medulla oblongata and nuclei of the cranial nerves. A similar picture is noted in the sympathetic ganglia, in particular, cervical (this is associated with hyperemia and puffiness of the face, hyperemia of the neck, injection of the vessels of the sclera). Significant damage occurs in the precapillaries of the skin and myocardium with the manifestation of exanthema and the development of myocarditis, respectively. The pathological process in the adrenal glands causes vascular collapse. In severe cases, deeper vascular damage with segmental or circular necrosis is possible. Thrombi form in the foci of vascular endothelial destruction, creating the preconditions for thrombophlebitis and thromboembolism.

Changes in organs can be characterized as typhus encephalitis, interstitial myocarditis, granulomatous hepatitis, interstitial nephritis. Interstitial infiltrates are also found in large vessels, endocrine glands, spleen, bone marrow.

The reverse development of morphological changes begins on the 18th-20th day after the onset of the disease and is completed by the end of the 4th-5th week, and sometimes at a later date.

The victims suffered from myocarditis, hemorrhages in the adrenal glands, enlarged spleen, edema, swelling and hemorrhages in the meninges and brain tissue.