Typhus: what's going on?

Pathogenesis of epidemic typhus

Gates of infection are minor skin lesions (often calculi). After 5-15 minutes, rickettsia enters the bloodstream, where some of them die under the action of bactericidal factors. And the bulk of pathogens penetrate into the endothelium of the vessels. In the cytoplasm of these cells, active reproduction of rickettsia occurs, which causes the swelling, destruction and desquamation of the endothelium with the development of rickettsiaemia. In the blood, a part of the rickettsia perishes, releasing endotoxin, another part of the microorganisms is introduced into the still intact cells of the endothelium of small vessels of different organs. This cycle without visible clinical manifestations is repeated until the body has accumulated enough rickettsia and their toxins, which will lead to the 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 circulating rickettsial endotoxin (LPS complex) in the blood renders the vasodilatory effect in the system of small vessels - capillaries, precapillaries, arterioles, venules, causing disturbance of microcirculation, up to paralytic hyperemia with a decrease in blood flow, a decrease in diastolic blood pressure, development of tissue toxic hypoxia and possible formation of DIC syndrome.

Pathomorphology of epidemic typhus

When multiplying rickettsia and killing endothelial cells, specific typhus-typhoid granulomas are formed.

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

• thrombus formation;
• destruction of wall vessels;
• cell proliferation.

Around the affected vessels in all organs and tissues, except for the liver, bone marrow and lymph nodes, there is focal cell proliferation, the accumulation of polymorphic cellular elements and macrophages with the formation of specific typhus-typhoid granules, called the Popov-Davydovsky nodules. Most of them 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 the nuclei of the cranial nerves. A similar picture is noted in sympathetic ganglia, in particular cervical (with this associated hyperemia and puffiness of the face, hyperemia of the neck, injection of vessels sclera). Significant lesions occur in 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 the collapse of blood vessels. In severe cases, a deeper lesion of the vessels with segmental or circular necrosis is possible. Clusters of vascular endothelial destruction form clots, creating prerequisites for thrombophlebitis, thromboembolism.

Changes in the organs can be described as typhoid fever 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 18-20th day after the onset of the disease and is completed by the end of the 4th-5th week, and sometimes even later.

The dead are noted myocarditis, hemorrhages in the adrenal glands, enlarged spleen, swelling, swelling and hemorrhage in the meninges and brain substance.