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Epidemic typhus (thyphus exanthematicus).

It refers to anthroponous rickettsiosis, is transmitted by lice, is characterized by generalized thrombovasculitis of small vessels and is manifested by severe intoxication, meningoencephalitis, hepatosplenomegaly and polymorphic roseole-petechial skin rash (exanthema). The disease is more often observed between the ages of 20 to 40 years. There is some predominance of men compared with women.

Brill’s disease is a recurrent (recurrent, sporadic) typhus that occurs in people who have had typhus in the past and who have survived rickettsia.

Etiology. The causative agent of epidemic typhus is rickettsia Provaceka (R. prowazekii).

Epidemiology. The source of the disease and the rickettsia reservoir is a sick person, it presents an epidemic danger from the last 2–3 days of the incubation period and up to 7–8 days after normalization of body temperature. The pathogen carrier is a worn (sometimes head) louse. When blood sucking, lice enter the digestive system along with the blood of the patient, rickettsia, which, having multiplied in the epithelium of the intestinal tube, are excreted with lice feces after 4 days. From this moment, lice become infectious and, upon changing the host, are able to infect a healthy person, secreting feces containing the pathogen next to the wound from the bite. Combing the itchy place, a person rubs lice with rickettsia in the feces wound. Thus, a transmissible pathway of infection with typhus is realized. Gates of infection - minor damage to the skin (often combs and wounds from bites of lice). A seasonal increase in the incidence in the winter-spring period is characteristic.

Currently, the disease is recorded mainly in developing countries in Africa, Asia, South and Central America.

Pathogenesis. Rickettsia have a tropism for vascular endothelium. They bind to cholesterol-containing receptors, are absorbed by the cell by endocytosis, enter the phagolysosomes and cytosol, followed by reproduction and destruction of the host cell. In this case, endotoxin and weak toxic substances are released, which activate kallikrein and kinins, causing local blood coagulation. Rickettsemia and destructive-proliferative thrombovasculitis of the vessels of the microvasculature with the development of typhoid granulomas around the damaged vessels lead to a variety of clinical symptoms. As a rule, the central and peripheral nervous system, skin, cardiovascular system, endocrine glands are affected. Rickettsia circulate in the blood throughout the febrile period of the disease and can persist for a long time in the body in a latent state in the cells of the mononuclear phagocyte system. Antibody-dependent and cellular variants of the immune system can prevent rickettsia reinfection, but they do not protect against typhoid reactivation after many years in the form of Brill-Zinsser disease. Activation of latent infection after exposure to any factors that weaken the immune system leads to a relapse of typhus - Brill’s disease, in which rickettsia again enter the bloodstream, damage the endothelium, determining the morphology and clinic of the disease. The course of the disease is much easier. If there is overwhelming in the patient’s environment with sporadic typhus, an outbreak of epidemic typhus is possible.

The clinical picture. The incubation period lasts from 7 to 21 days (usually 12-14 days). The disease begins acutely and is manifested by chills, decreased appetite, severe headache, fever up to 38.5–39.0 ° С, which does not decrease until the 8-14th day of illness (in untreated patients). From the first days of the febrile period of the disease, headache, insomnia, agitation, and increased sensitivity to light and sound stimuli appear. Hyperemia of the face, neck, upper torso, conjunctiva and vascular injection of the sclera (red eyes on a red face) are noted. On the third day of the disease, hemorrhages can be detected on the transitional fold of the conjunctiva - purple-bluish spots of Chiari-Avtsyn, on the mucous membrane of the soft palate and tongue - petechiae (Rosenberg enanthem), the latter are detected in 90% of patients. Symptoms of damage to the cranial nerves appear. From the 3-4th day of the disease, the liver and spleen increase. On the 4th – 6th day, a polymorphic roseole-petechial rash appears on the trunk (mainly on the lateral surfaces) and limbs. Roseola vary in size (from 0.2 to 0.5 cm), shape, color intensity. The face, palms, and soles are usually free of rash. Petechiae can be observed located both in the center of the roseola (secondary) and separately from them (primary). Roseola resolves after 3-5 days, and petechiae after 7-8. During the rash, the patient's condition worsens: the headache intensifies and takes on a bursting pulsating nature. Auditory, visual, olfactory hallucinations, delusions of awesome content can occur. Consciousness is disturbed, focal (bulbar) and cerebral (meningeal) symptoms appear.

From almost 4-6 days, an increase in the liver is detected in almost all patients, and in the spleen, in 50-60%.

Common vasculitis in combination with innervation disorders reduce tissue resistance, patients quickly form necrosis and pressure sores. Damage to the central and peripheral (sympathetic) nervous system, myocardium and adrenal glands leads to severe hypotension and even death from accruing cardiovascular failure.

The duration of the disease depends on its severity. With a favorable course, body temperature normalizes to the 8-14th day of illness. The period of convalescence is long, the ability to mental work is restored gradually. With antibiotic therapy, a febrile period can be reduced to 24–48 hours, which facilitates the course of the disease.

Pathological anatomy. When autopsies of typhus died of typhus, pathognomonic (characteristic) symptoms cannot be identified, and the diagnosis can only be assumed. Major changes are detected only by microscopic examination of organs.

During an autopsy, typhoid fever will be indicated by: traces of a rash on the skin and conjunctiva; plethora of cerebral vessels; dull pia mater on convex parts of the hemispheres (serous meningitis); splenomegaly (spleen mass can reach 300-500 g), and the spleen tissue is soft, full-blooded, gives a small scraping of the pulp; pressure sores.

A microscopic examination reveals signs of a characteristic vascular disease of the microvasculature - typhoid vasculitis.
The range of lesions is quite wide and includes: swelling, destruction and desquamation of the endothelium with the formation of blood clots (parietal or obstructive); proliferation of endothelium and adventitia cells; the appearance of inflammatory infiltration (lymphocytes, macrophages, single neutrophils); damage to the walls of blood vessels up to fibrinoid necrosis. The listed changes can be expressed to varying degrees and different combinations. Depending on this, the following types of typhoid vasculitis are distinguished: warty, endovasculitis, proliferative and necrotic. If the whole complex of vascular changes is observed, they speak of destructive-proliferative endotrombovasculitis.

Inflammatory infiltration of the vessel wall has a focal character, with the formation of rounded compact cellular nodules - granulomas. Granulomas were first discovered in a patient with typhus in the central nervous system and described by L.V. Popov in 1875. Syndrome typhoid granulomas are found in all tissues, with the exception of the organs of the reticuloendothelial system (liver, spleen, lymph nodes, bone marrow). The formation of granulomas involves the endo- and perithelium of capillaries, adventitious arteriole and venule cells, lymphocytes surrounding the vessel, and single neutrophils. In the center of the formed granuloma, the lumen of the vessel is hardly recognized or not detected at all among the cells.

In the central and peripheral nervous system, the structure of granulomas has some features: they are surrounded by a wide area of ​​proliferating microglia. In the brain, typhoid granulomas usually appear in the second week of the disease and exist for about four weeks. They are found in the bridge and legs of the brain, subcortical nodes, medulla oblongata (usually at the level of the lower olives), the posterior lobe of the pituitary gland. In the white matter of the hemispheres, nodules are absent. In addition to granulomas, cerebral congestion of blood vessels, stasis, perivascular (perivenous) couplings from plasma cells, focal glial proliferation are noted. Dystrophic changes in neurons are moderate. Thus, encephalitis develops in the brain, which is often combined with serous meningitis (see above). In the sympathetic nervous system, inflammatory changes are formed, both granulomatous and with the formation of lymphoid cell infiltrates, plethora, dystrophic changes in neurons, i.e., typhoid ganglionitis develops. Inflammatory changes are also found in the peripheral nervous system, where neuritis develops.

A large number of typhoid granulomas around the vessels of the microvasculature and small arteries in the surface layers of the dermis are determined in the skin. With the predominance of necrotic vasculitis, hemorrhages (petechiae) can appear.

The heart is constantly damaged, which is expressed in the form of damage to cardiomyocytes and / or the development of interstitial myocarditis (possibly focal and diffuse spread of infiltrate, the formation of nodules).

Vessels (arteries) of large, medium and small caliber are often affected by typhus. The defeat is manifested by endothelial necrosis, sometimes by segmental necrosis of the muscle membrane with subsequent parietal or obstructive thrombosis and local hemodynamic disorders (gangrene of the extremities, foci of necrosis in the brain, retina).

Changes develop in the endocrine glands. In the thyroid gland there is an interstitial inflammation - thyroiditis. In the adrenal glands, endotrombovasculitis typical of typhus is formed, leading to hemorrhages and foci of necrosis.

In the remaining organs, lymphomacrophagic and plasmocyte infiltrates, hemorrhages are intermittently met.

Typhoid fever complications are caused by vascular and nervous system damage. In connection with damage to the pressor systems of the body and myocardium, patients have a persistent tendency to hypotension. Often develop trophic disorders in the skin. From slight pressure there are gangrene of the limb, auricle and bedsores (in the heels, sacrum, spinous processes of the vertebrae, on the skin of the finger from the ring). In connection with the defeat of the cervical sympathetic nodes and inhibition of secretion of the salivary glands, conditions are created for the development of secondary infection (purulent mumps, otitis media). With subcutaneous injections of drugs and spontaneously, foci of subcutaneous fat necrosis - oleogranulomas - may appear. As a result of circulatory and ventilation disorders in the lungs, bronchopneumonia develops. As a result of damage to the vessel wall and cardiovascular failure, thrombophlebitis may develop. Adjoining secondary infection can lead to the development of phlegmon and, in severe cases, to septicopyemia.

Typhus death occurs as a result of increasing cardiovascular failure or from bacterial complications (generalization of a secondary infection and the development of sepsis). The highest mortality rate is observed in people older than 40 years. Typhus in children is easy, mortality is low.

Sporadic typhus (Brill-Zinsser disease) - etiologically identical to epidemiological typhus, are a type of disease. It occurs in a population that previously had typhus and is considered a relapse. Typhoid fever is characterized by the appearance of single cases of the disease, mainly in people older than 45 years, a benign course, lack of pediculosis, a high titer of antibodies to the specific Rickettsia antigen Provaceca. Clinical manifestations and the nature of morphological changes are similar to those in epidemic typhus, but are less pronounced. Mortality does not exceed 0.8%.

The occurrence of sporadic typhus indicates the presence of people who have had epidemic typhus, a Provackec rickettsia reservoir (endocytobiosis) and the possibility of recurrence of the disease after years of remission. If there is overwhelming in the patient’s environment with sporadic typhus, an outbreak of epidemic typhus is possible.

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