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Tick-spotted spotted fever

The group of tick-borne spotted fevers combines the Rocky Mountain spotted fever, Marseilles fever, Volyn fever, vesicular rickettsiosis, tick-borne typhus of North Asia and others. Tick-borne typhus of North Asia is most widespread in the USSR.

Tick-borne loose typhus of North Asia

Tick-borne rash typhus in North Asia (North Asian tick-borne rickettsiosis, tick-borne rash typhus, etc.) is an acute infectious disease with a benign course characterized by the presence of primary affect, fever and skin rashes. The disease was first described in our country in 1934 in the Far East by E.I. Millem.

Etiology . The disease is caused by Rickettsia sibirica, which can multiply in the yolk sacs of chicken embryos and in tissue cultures.

Epidemiology . Tick-borne typhus is registered in Siberia, the Far East, Northern Kazakhstan and others. This is a natural focal zoonosis. The reservoir of infection is small rodents (ground squirrels, field mice, chipmunks hamsters, etc.). Transmission of infection from infected rodents to humans is carried out exclusively through ticks. The highest incidence is recorded during the activity of ixodid ticks - the spring-summer period of the year.

Pathogenesis not studied.

Clinical picture . At the site of a tick bite, after 3-5 days, primary affect occurs in the form of an inflammatory reaction of the skin with lymphadenitis. At the same time, body temperature rises, chills, malaise, headaches and muscle aches appear. Before the temperature rises, prodromal phenomena can be noted: chilling, malaise, loss of appetite. The temperature reaction reaches a maximum within 2-3 days, can be remitting, lasts about 5-10 days. At the height of the fever (usually on the 2nd-3rd day of the disease), an abundant polymorphic resoleous-papular rash appears, mainly on the trunk and around the joints. In severe cases, a rash occurs throughout the body, including on the face and soles of the feet. Sometimes the rash is with a hemorrhagic component.

The most characteristic sign of tick-borne typhus is primary affect. Usually it is found on open parts of the body: the head, neck, shoulder girdle and is a dense, painful infiltrate, covered with a brown crust surrounded by a zone of hyperemia. As a rule, regional lymphadenitis accompanies primary affect.

Tick-borne typhus is characterized by hypotension, bradycardia, moderate enlargement of the liver and spleen. The patient's face is hyperemic, slightly puffy. Constantly observed hyperemia of the mucous membranes of the tonsils, soft palate, arches. Sometimes there is an enanthem. In the blood, moderate neutrophilic leukocytosis, lymphopenia, ESR increased. Sometimes there are atypical forms of the disease - without primary affect, regional lymphadenitis or without rashes.

Flow benign disease. Recovery begins on the 7-14th day of illness.

The disease in children of the first years of life is rare due to the limited possibility of attack by ixodid ticks. The disease is relatively easy, but severe cases with a fatal outcome are also possible.

Diagnosis . In typical cases, the diagnosis does not present great difficulties. It is put on the basis of the presence of primary affect, regional lymphadenitis, fever, characteristic rashes and epidemiological data (natural focus of infection). To confirm the diagnosis, RSK and RNGA are used. Specific antibodies appear from the 5-6th day from the onset of the disease and reach a maximum at 3-4 weeks.

Treatment . Apply tetracycline antibiotics 0 age-specific dosage for 7-10 days.

Prevention . Individual and collective protection of children from tick attacks, timely removal of ticks from the body, wiping the bite with alcohol or iodine solution.

Marseille fever is an acute infectious disease characterized by the presence of primary affect at the site of a tick bite, regional lymphadenitis, fever, maculopapular rashes.

Etiology . The causative agent of the disease Rickettsia conorii was discovered in 1932. Some types of dog ticks are the natural reservoir and carrier of the pathogen, which preserve rickettsia for life and transmit them to their offspring transovarially.

Epidemiology . Human infection occurs when ticks bite or crush them, followed by rubbing rickettsiae into damaged skin and mucous membranes. Human-to-human transmission has not been established. On the territory of our country, foci of Marseille fever are recorded in the Crimea, on the Black Sea coast of the Caucasus, the Absheron peninsula and in the coastal regions of Dagestan.

Pathogenesis . At the site of a tick bite, after a few hours, a pathological focus occurs - the primary affect. From the primary focus, the pathogen reaches the regional lymph nodes via the lymphogenous pathway, where the inflammatory process often occurs - lymphadenitis. The next stage is characterized by the generalization of infection with the penetration of rickettsia into the endothelium of small vessels, which leads to the development of specific 'vascular granulomatosis (panvasculitis). The severity of vascular changes correlates with the severity of the disease.

Clinical picture . The incubation period lasts an average of 5-7 days, sometimes it can be extended to 18 days. The disease begins acutely with a rise in body temperature to 38-40 ° C, chills, headache and muscle pain. General lethargy, sleep disturbance, vomiting is possible. The patient's face is moderately hyperemic, the scleral vessels and conjunctiva are injected, hyperemia of the mucous membrane of the pharynx is often noted, sore throat is possible. The tongue is coated with a gray coating. During the whole illness, the primary affect remains on the skin, which is an inflammatory, dense infiltrate with central necrosis, and then a scab of black, brown color, surrounded by a zone of hyperemia with a diameter of up to 5-7 mm. The crust disappears after normalization of body temperature, the ulcer formed at the site of the scab is epithelized in the period of convalescence (at the 3-4th week of illness). In the zone of primary affect, regional lymphadenitis occurs, while the lymph nodes can be large (up to 5-10 cm in diameter), painful on palpation.

A characteristic feature of Marseille fever is a rash. Usually it appears on the 2-3rd day of the disease, first on the body, and then throughout the body, including the face, palms and soles. The rash is initially spotty, then becomes spotty-papular, sometimes transforming into red acne-like formations (“acne-like fever”), often with a hemorrhagic component in the center of individual elements. The rash lasts throughout the febrile period with a gradual fading. At the site of the rash, skin pigmentation may persist for 1-2 months.

At the height of the clinical manifestations, most patients have relative bradycardia, deaf heart sounds, the spleen is often enlarged, less often the liver. In severe cases, the phenomena of meningitis, delirium, tremor of the tongue, hands are possible. Leukopenia with relative lymphocytosis and a slight increase in ESR are noted in the blood.

More often mild and moderate forms with a favorable course are observed. Severe cases are rare. Atypical forms of the disease are possible - without rash, primary affect, and regional lymphadenitis.

Forecast . With Marseilles fever, the prognosis is favorable. Complications are rare, fatal cases do not occur.

Diagnosis . Diagnosed on the basis of the patient’s primary affect, maculopapular rash, fever, as well as the child’s presence in the endemic focus.

For laboratory confirmation of the diagnosis, RSK, RNGA are used using the whole D. conorii antigen. To isolate rickettsia from the blood of patients or ticks, intraperitoneal administration of the material to male guinea pigs is used, and the development of periorchitis confirms the diagnosis.

Marseille fever must be differentiated from drug allergies and other rickettsioses.

Treatment . As a means of etiotropic therapy, chloramphenicol, tetracycline in an age-specific dosage throughout the entire febrile period and another 2-3 days at normal body temperature are used. Antihistamines, anti-inflammatory and other symptomatic drugs are indicated.

Prevention . The fight against ticks in endemic foci (treatment with acaricidal preparations of dogs, dog kennels and other places of probable reproduction of ticks).


Tsutsugamushi fever is an acute rickettsial disease characterized by fever, maculopapular rash and the presence of primary affect. In the Soviet Union, the disease occurs in the southern regions of the Primorsky Territory and some areas of the Tajik SSR.

Etiology . The causative agent of the disease - R. tsutsugamushi - was first isolated by Japanese authors in 1930. Under natural conditions, it parasitizes in the larvae of red-tick mites, characterized by transovarian transmission of the pathogen, as well as in the organism of small rodents. A person becomes infected during a stay in a natural focus.

Clinical picture . The disease develops 1-3 weeks after the bite of an infected red-mite tick. By the end of the incubation period, the appearance of prodromal phenomena is possible: malaise, headache, loss of appetite. More often, the disease begins acutely with a rise in body temperature, chills, headache. From the first day of the disease, primary affect appears at the site of the tick bite. Usually these are closed parts of the body in places of natural skin folds: inguinal, axillary, perineal, etc. The evolution of primary affect is characteristic: first a hyperemic and weakly infiltrated spot appears, then it quickly turns into a vesicle and finally into a sore.

A flat ulcer is surrounded by a zone of hyperemia and is covered with a brown crust. Regional lymphadenitis is characteristic. The fever reaches its maximum on the 2nd-3rd day of the disease, has a remitting character and lasts about 2-3 weeks. The patient's face is slightly hyperemic, sclera is injected with conjunctivitis. On the 3-6th day of the disease, an abundant maculopapular rash appears, more on the trunk and limbs.

Flow the disease is usually benign. The rash disappears after 5-10 days. Healing of an ulcer is noted at the 2-3rd week of illness.

Diagnosis . Tsutsugamushi fever is diagnosed on the basis of prolonged fever, the appearance of a maculopapular rash, the presence of primary affect with regional lymphadenitis and the patient's presence in the endemic focus. To confirm the diagnosis, RSK with antigens of the pathogen are put. Retains diagnostic value and RA with Protein OX19 (the causative agent has a common O-antigen with OX protein19).

Treatment . Assign chloramphenicol in an age-related dosage until the body temperature is completely normalized.

Prevention same as with other tick-borne rickettsioses.


Q fever (Central Asian fever, typhoid fever, etc.) is an acute rickettsial disease that occurs with fever, frequent damage to the central nervous system and the development of specific pneumonia.

The disease is ubiquitous. On the territory of the USSR it is found mainly in the southern regions of the country. The first description of the disease was made in 1937 by E. N. Derrick. In the same year, F. M. Burnet and M. Frieman isolated the pathogen from the blood of patients.

Etiology . Unlike other rickettsia, the causative agent of Q fever - Coxiella burneti - does not have common antigens with the protein.

In vivo, infection is found in many mammals, birds, ticks. Warm-blooded animals are a temporary carrier of C. burneti, while ixodid ticks transmit the pathogen transovarially to their offspring. Domestic animals that become infected in foci of infection from wild animals and infected ticks can also be involved in the process of C. burneti circulation.

Epidemiology . Infection of a person can occur alimentary by eating food (milk, egg, etc.) from infected animals or by airborne droplets when inhaling dust containing secretions of infected animals (when processing wool, skin, fur, etc.), in contact with infected domestic animals, etc. The infection of a healthy person from the patient is not observed.

Pathogenesis . Q fever is an infectious benign reticuloendotheliosis without the development of endovasculitis. Rickettsia propagation occurs mainly in SMF cells and to a lesser extent in vascular epithelial cells. The greatest changes are found in the lungs, cardiovascular system, liver and spleen.

Clinical picture . The clinic is characterized by polymorphism. The incubation period averages 15-20 days. The disease begins acutely with a rise in body temperature to high numbers, fatigue, weakness, feelings of heat, headache, sweating. From the first days of the disease, hyperemia and puffiness of the face, vascular injection of the sclera, hyperemia of the mucous membranes of the tonsils, soft palate, and often enanthema appear. Often, changes in the respiratory system are detected at the height of the disease: tracheitis, tracheobronchitis or bronchitis, the development of focal pneumonia, rarely pleuropneumonia, is characteristic. The course of pneumonia is torpid. In all patients, headache, insomnia, instability of the psyche are noted, hallucinations are possible. Pain in the eyeballs and muscle pain are characteristic. Some patients complain of abdominal pain, they may have an upset stool. In half of the patients, the size of the liver and spleen is increased. In severe cases, the development of serous meningitis and encephalitis is possible.

The leading symptom in Q fever is a prolonged increase in body temperature. Usually a fever is persistent or remitting in nature and is accompanied by sweats, often chills. Its duration is from several days to 3-4 weeks or more.

There are mild, moderate and severe forms of the disease. In the foci of infection, erased and subclinical forms are often recorded.

The course of the disease can be acute (up to 2-3 weeks), subacute - up to 1.5 months and chronic - up to 1 year.

Diagnosis . Q fever can be suspected in the endemic focus on the basis of a prolonged increase in people’s temperature, accompanied by sweats, muscle and headaches, arthralgia. For final diagnosis, laboratory confirmation is required. Use PH, CSC, skin allergy test. Isolation of C. burneti from blood, sputum, urine, cerebrospinal fluid is of great importance. Guinea pigs, white mice or cotton rats are infected with material from patients. Burnet's rickettsia in large quantities accumulate in the liver, spleen and other organs of infected animals.

Treatment . Prescribe antibiotics from the group of tetracycline and chloramphenicol in an age-specific dosage for 7-10 days and symptomatic agents.

Prevention . Preventive measures are aimed at exterminating ticks in nature, protecting domestic animals from tick attacks, and strict observance of quarantine measures against sick animals. Of great importance is the educational work among the population, especially in endemic foci. It is important to strictly observe the rules of personal prophylaxis when caring for sick pets. Milk is allowed only after boiling. For active immunization, the live vaccine M-44 is proposed, which is administered strictly according to epidemiological indications.

A source: Nisevich N.I., Uchaykin V.F. Infectious diseases in children: Textbook.- M.: Medicine, 1990, -624 p., Ill. (Textbook. Lit. for student. Medical. In-com. Pediatric. Fact.)


The disease was first detected in our country in 1934-1935.in the Far East by the Soviet military doctor E.I. Mill. In 1936-1937 it was described by N.I. Antonov and A.G. Neishtat under the name "Far Eastern rash tick-borne fever." Twice, in 1938 and 1940, the disease was studied by an expedition led by M.K. Krontovskaya. The wedge is most complete, a picture of S. to. described by N. V. Sergeev (1940-1944), and then S. M. Kulagin and G. I. Feoktistov. The name of the disease "tick-borne rickettsiosis" was given by MK K. Krontovskaya in 1940


The causative agent of S. to.- Rickettsia sibirica Zdrodovskii et Golinevich, 1948, belongs to this. Rickettsiaceae. Rickettsia (see) are localized in a cytoplasm and in a nucleus of cells. The size of the pathogen 0.7—2.5> Epidemiology

S. to. R. - a natural focal zoonosis (see). The source of the pathogen is small rodents - ground squirrels, field and forest mice, house mice, hamsters, chipmunks, gray rats, pestles, Far Eastern and red-gray voles. The pathogen is transmitted by ixodid ticks of various species - Dermacen-tor nuttali, D. silvarum, D. marginatus, and others, which live in steppe and meadow shrub thickets. A person becomes infected as a result of an attack by ticks in the natural focus of the disease (see Natural focality), rickettsia is transmitted with tick saliva. Sporadic incidence (0.29-1.8 per 100 thousand inhabitants) is recorded in the spring-summer period, which is associated with the activity of ixodid ticks at this time of the year.

Pathogenesis and pathological anatomy

The determining factor in the pathogenesis of the disease is the vasodilating effect of the rickettsia toxin and parasitization of rickettsia in the vascular endothelium, which causes inflammatory changes in them, while proliferative processes prevail over destructive ones with the development of endo-perivasculitis. Feature S. to. consists in the fact that pathomorphological changes are most pronounced in the vessels of the skin, less in the vessels of the brain and other organs.

Immunity after a disease is usually long, repeated diseases are not observed.

Clinical picture

The incubation period ranges from 2 to 7, usually 3-6 days. Prodromal phenomena are noted within 1-3 days. in the form of malaise, fatigue, vague muscle pain and chills. Depending on the severity of symptoms, the disease can occur in mild, moderate. or severe form.

More often a moderate form is observed. The disease usually begins acutely with an increase in temperature, the appearance of a headache, a feeling of heat with chills, sweating, pain throughout the body, including joints and muscles, general weakness, sometimes inflammatory changes in the upper respiratory tract, sleep disturbances, and poor appetite . These symptoms, gradually increasing, persist throughout the entire febrile period (see. Fever). The temperature in the first two days reaches 39-40 ° and more often is remitting, it usually decreases lytically. The duration of the febrile period is from 1 to 20 days, depending on the severity of the disease, usually 7-10 days. After several days of lowering the temperature, it may increase within two to five days, which is regarded as a result of difficult to diagnose pulmonary complications. The patient's face is often hyperemic and somewhat puffy already from the 2nd – 3rd day of illness. Almost constantly hyperemia of the mucous membrane of the soft palate, tongue and tonsils is detected, sometimes even with enanthema (see Rashes) along the edges of the arches and at the base of the tongue.

The most constant and typical signs of the disease are primary affect (see Primary affect), which occurs at the site of a tick bite and is accompanied by regional lymphadenitis, K-rats are detected on average in about 80% of patients. The primary affect is a dense, painful infiltrate, covered with a brown necrotic crust and surrounded by a pink border of hyperemia on the periphery. Polymorphic abundant roseola-papular rash on the body appears on the 2nd-4th day of illness. The most intense rash in the joints. Rash is not accompanied by itching. In the first 1-2 days, roseola and less often papules are spilled. Later roseols turn into papules and very rarely in petechiae.

Disorders of the cardiovascular system are expressed in early-appearing relative bradycardia, hypotension and a decrease in pulse pressure, moderately expressed interstitial myocarditis. Disturbances of c are characteristic. n from. Headache, usually diffuse, occurs in all patients, is intense in the first 5-6 days, often accompanied by insomnia or intermittent sleep. Sometimes meningism is detected (see) with an increase in cytosis in the cerebrospinal fluid (see) up to 30-50 leukocytes in 1 μl (mainly lymphocytes) and protein up to 0.9 g / l. Catarrhal phenomena of the upper respiratory tract and bronchi are observed, but there are no changes in the lungs. Appetite decreases, nausea and vomiting, diarrhea are possible. The tongue is moist, slightly coated with a white coating. The abdomen is soft and very rarely painful (an increase in mesenteric nodes). In most patients, the liver and spleen increase. The recovery period begins after 9-11 days from the onset of the disease.

With a mild form, the febrile period lasts up to 7 days, the temperature is not higher than 38 ° C, the condition of the patients is satisfactory, a moderate rash, mostly rose-colored, there are no complications.

For the severe form, usually observed in older people, fever lasting up to 20 days with a temperature of 39–41 ° C and above is characteristic, symptoms of C. n from. and the cardiovascular system, an abundant papular rash with a tendency to hemorrhagic transformation of elements.

An atypical course of the disease is sometimes noted - without primary affect, regional lymphadenitis or rash, perhaps the course is erased when the wedge, the picture is not enough expressed.

Complications rare, sinusitis, otitis media, laryngitis, bronchitis, pneumonia occur.


The diagnosis is based on epidemiol data. anamnesis (the patient’s presence in the focus of S. to. r., tick bites, seasonality, a short incubation period after a tick bite) and on the wedge, the picture. Normocytosis and moderate leukopenia with eosinopenia, neutropenia and relative lymphocytosis are noted in the blood. To confirm the diagnosis, CSCs and an indirect hemagglutination reaction (PHHA) are used, which become positive from the 5-7th day of the disease, less often from the 9-11th day, CSC titers are low - 1: 40-1-160, RNGA - 1: 800-1: 3200, DSC remains positive for a long time.

Treatment, Prognosis, Prevention

Treatment is with tetracycline preparations.

The prognosis is favorable even in severe cases of the disease.

Prevention The main event is the individual protection of people from tick attacks: when working on the territory of natural foci of S. to. protective clothing is used (see tick-borne encephalitis) and Pavlovsky's repellent nets impregnated with repellents (see Protective nets), self and body inspections of clothes and clothes after each visit to tick mites, removal of sucked mites, rubbing of the bite with alcohol or iodine .

Specific prevention is not developed.

Bibliography: Zdrodovsky P.F. and Golinovich E. M. The doctrine of rickettsias and rickettsioses, M., 1972, Loban K.M. Clinic and diagnosis of some endemic rickettsioses, p. 47, M., 1977, aka, The most important human rickettsioses, L., 1980, Lyskovsky, M. M. Tick-borne rickettsiosis, M., 1963, bibliogr., General and private epidemiology , ed. I.I. Elkina, vol. 2, p. 162, M., 1973, Guide to Infectious Diseases, ed. A.F. Bilibin and G.P. Rudnev, p. 489, M., 1962.

Tick-borne typhus in North Asia

Synonyms: tick-borne rickettsiosis, tick-borne typhus fever, tick-borne typhus of the East, eastern typhus, typhus-borne typhus of Siberia.

Tick-borne typhus of North Asia is an acute benign natural focal obligate-transmissible rickettsiosis, characterized by the presence of primary affect, febrile reaction, maculopapular rashes on the skin, enlargement and soreness of regional lymph nodes.

The disease was first described by E. I. Mill in Primorye in 1936. The etiology, epidemiology and clinic were studied in detail since 1938 by special expeditions led by E. N. Pavlovsky. The causative agent was isolated by O.S. Korshunova in 1938 from the cytoplasm of cells of a necrotic focus on the skin of a patient that arose after suction of an ixodid tick (Yatsimirskaya-Krontovskaya M.K., 1940).

Etiology and epidemiology .

The causative agent of tick-borne rickettsiosis Rickettsia sibirica belongs to the genus Rickettsia family Rickettsiaceae , has similarities with other rickettsiae, multiplies in the cytoplasm and nucleus of affected cells.

In the foci of the disease, pathogen circulation occurs between wild mammals and ixodid ticks (Dermacentor, Haemaphysalis, Ixodes ) - natural and main reservoirs R. sibirica . In ticks, transovarial and transphase transmission pathways of rickettsia are observed. Infection of a person with tick-borne typhus occurs in natural foci through the bite of infected ticks, the saliva of which contains rickettsia.

Tick-borne typhus is a seasonal disease. The maximum incidence is observed in spring and early summer, due to the period of the highest tick activity. In autumn, a second rise in incidence is possible, determined by the second generation of arthropods. Sporadic diseases are found mainly in agricultural workers. The range of tick-borne typhus typhus extends from the Urals to the shores of the Pacific Ocean, including the Far East, Transbaikalia, Siberia, Altai Territory, Kazakhstan and Kyrgyzstan, as well as the eastern part of Mongolia.

Pathogenesis and pathological anatomy .

At the site of the entrance gate of infection, primary affect occurs - an inflammatory reaction of the skin with regional lymphadenitis. The causative agent is introduced into the endothelium of small vessels, causing inflammatory changes in them. Moreover, proliferative processes prevail over destructive ones with the development of endoperivasculitis, which explains the milder course of the disease compared with epidemic typhus. Rickettsiemia and toxinemia with tick-borne rickettsiosis cause symptoms of intoxication.

The incubation period lasts 4-7 days. The disease begins acutely: chills appear, body temperature quickly rises to 39–40 ° C. Less commonly observed is the prodromal period in the form of malaise, headache and muscle pain, loss of appetite. Often there is hyperemia of the face, neck, mucous membrane of the pharynx, as well as enanthema.

At the end of the incubation period at the site of a tick bite on the open parts of the body (scalp, neck, shoulder girdle), primary affect occurs, which is a dense infiltrate, slightly painful on palpation. In its center is a necrotic crust of dark brown color, on the periphery there is a red rim of hyperemia. Infiltrate reaches 1–2 cm in diameter. Remitting fever, less often of constant type, lasts on average 8-10 days (sometimes 20) and ends lytically. Depending on the severity of the phenomena of intoxication, mild, moderate and severe forms of tick-borne rickettsiosis are distinguished.

Leading in the clinical picture of the disease are the symptoms of damage to the nervous system in the form of a persistent, sometimes excruciating headache, pain in the muscles and lower back. Unlike epidemic typhus with tick-borne typhus statustyphosus is absent. Meningeal symptoms are occasionally detected. Conjunctivitis and scleritis, bradycardia and hypotension are noted.

A persistent symptom is a rash that appears on the 2nd-5th day of illness. In most patients, it first appears on the trunk, and then extends to the limbs, where it is localized mainly on the extensor surface and around the joints. With an abundant rash, the elements of the rash can be on the face, palms, soles. The rash is polymorphic and has a predominantly roseole-papular character. A more severe course of the disease is accompanied by hemorrhagic rashes. After a few days, the rash gradually dies away, remaining the longest in the region of the lower extremities and buttocks of convalescents, brownish pigmentation remains for a long time in place of individual elements of the rash.

Moderate neutrophilic leukocytosis, lymphopenia are found in the blood, ESR is increased. The disease is benign, relapses are not observed.

Diagnostics and differential diagnostics .

Specific diagnosis involves the isolation of a pure culture R. sibirica from the patient’s blood using guinea pigs (scrotal reaction). Serological diagnosis is carried out using RSK using a whole antigen from R. sibirica . Diagnostic titers are low (1: 40-1: 60). In the acute period, at a high level of hemagglutinins (1: 800–1: 13,200), RNGA gives positive results. An additional method is the Weil-Felix reaction with the OX19 antigen, positive in 80% of patients.

Tick-borne rickettsiosis is differentiated from epidemic typhus, Brill's disease, rat typhus and other rickettsioses from the group of tick-borne spotted fever.

Treatment and prevention .

Treatment is successfully carried out with tetracycline antibiotics in a hospital. Along with antibiotics, symptomatic agents are used.

Prevention is protection against tick attacks.