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Astrakhan rickettsiosis fever: causes, symptoms, diagnosis, treatment

 
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Last reviewed: 05.07.2025
 
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Astrakhan rickettsial fever (synonyms: Astrakhan spotted fever, Astrakhan fever, Astrakhan tick-borne spotted fever) is a rickettsiosis from the group of spotted fevers, transmitted by the tick Rhipicephalus pumilio and characterized by a benign course, the presence of a primary affect, fever, and a maculopapular rash.

ICD-10 code

A77.8 Other spotted fevers.

Epidemiology of Astrakhan rickettsial fever

The main epidemiologically significant factor in the foci of Astrakhan rickettsial fever is the constant and fairly extensive infestation of dogs with the tick Rhipicephalus pumilio, the main reservoir and carrier of rickettsia. Not only stray dogs are affected by the tick, but also animals kept on a leash and guard dogs that do not leave their yards. Significant infestation with R. pumilio ticks has been found in wild animals (for example, hedgehogs and hares). Ticks can crawl from dogs, from the surface of the soil and plants to humans. Ticks are unevenly distributed across the region depending on the microclimate, landscape, number and nature of the settlement of hosts: hedgehogs, hares, etc. Several decades ago, the R. pumilio tick was rarely found on farm and domestic animals, although the number of affected wild animals and the degree of their tick infestation in the Northern Caspian region were high. Due to anthropogenic impact (industrial development of the Astrakhan gas condensate field, construction and commissioning of two stages of the gas condensate plant), a low-activity natural focus of previously unknown rickettsiosis turned into a manifest natural-anthropurgic focus of Astrakhan rickettsiosis fever.

Ticks retain rickettsiae for life and transmit them transovarially. A person becomes infected when a tick attaches. Infection is possible by contact when rubbing the hemolymph of a crushed tick, its nymph or larva into damaged skin, mucous membranes of the eyes, nose, or through an aerosol suspension. Natural susceptibility to Astrakhan rickettsial fever is of all ages. Residents of rural areas of the Astrakhan region are most often affected: adults of working age and the elderly (work in vegetable gardens, summer cottages, in agriculture), children of preschool and primary school age (greater contact with domestic animals). The disease is seasonal: April-October with a peak incidence in July-August, which is associated with an increase in the number of ticks at this time, mainly its juvenile forms (nymphs, larvae). The incidence of Astrakhan rickettsial fever has also been detected in regions adjacent to the Astrakhan region, in particular in Kazakhstan. Cases of Astrakhan rickettsial fever have been noted among vacationers in the Astrakhan region after their departure.

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What causes Astrakhan rickettsial fever?

Astrakhan rickettsial fever is caused by Rickettsia conori, var. casp., which does not differ from other representatives of the group of spotted fever pathogens in morphological and tinctorial properties. Rickettsia parasitize in the cytoplasm. As shown by electron microscopy methods, the length of the rickettsia is 0.8-1 μm, the cell is surrounded by two three-layer membranes. They are cultivated in tissue culture, as well as in the yolk sac of a developing chicken embryo and in affected mesothelial cells of laboratory animals (golden hamsters). A detailed analysis of the molecular genetic characteristics of the rickettsia that cause Astrakhan rickettsial fever allows them to be differentiated from other pathogens of the rickettsioses of the ASF group.

Pathogenesis of Astrakhan rickettsial fever

At the site of tick attachment, the pathogen begins to multiply and the primary affect is formed. Then, rickettsiae penetrate into regional lymph nodes, where they also reproduce, accompanied by an inflammatory reaction. The next stage is rickettsiaemia and toxinemia, which form the basis of the pathogenesis of Astrakhan rickettsial fever. Morphologically, necrotic damage to the epidermis, neutrophilic microabscesses of the papillary layer of the skin are observed in the primary affect. Acute vasculitis of vessels of different diameters with pronounced swelling of the endothelium, in places with fibrinoid necrosis, destruction of the elastic framework, swelling of the collagen fibers of the dermis develops. Enlarged lumens of vessels are noted, some vessels contain thrombi. Vasculitis is initially local, within the primary affect, and with the development of rickettsiaemia it becomes generalized. The vessels of the microcirculatory bed are mainly affected: capillaries, arterioles and venules. Disseminated thrombovasculitis develops.

Hemorrhagic elements are caused by perivascular diapedetic hemorrhages. By the beginning of recovery, basal keratocytes begin to proliferate in the epidermis; hyperpigmentation develops as a result of the breakdown of erythrocytes and hemoglobin; infiltration and swelling of the endothelium decrease; smooth muscle elements of the vascular wall proliferate; fibrinoid swelling of collagen fibers and edema of the dermis gradually disappear.

Rickettsia disseminate into various parenchymatous organs, which is clinically manifested by an enlargement of the liver, spleen, and changes in the lungs.

Symptoms of Astrakhan rickettsial fever

There are four periods of the disease:

  • incubation;
  • elementary;
  • height;
  • convalescence.

Astrakhan rickettsial fever has an incubation period that ranges from 2 days to 1 month.

The first symptoms of Astrakhan rickettsial fever are the primary affect at the site of tick attachment. Frequency and duration of individual symptoms in patients with Astrakhan rickettsial fever

Symptom

Number of patients, %

Duration of symptoms, days

Fever

100

9-18

Weakness

95.8

12

Headache

88.5

10

Dizziness

33 9

7

Insomnia

37 5

7

Conjunctivitis

42.7

7

Scleritis

45.8

7

Hyperemia of the pharynx

70.8

8

Hemorrhages into the mucous membranes

151

6.5

Hemorrhagic rash

41.7

11

Rash maculopapular-roseolar

100

13

Rash with persistent pigmentation

59.9

11.5

Rash localization: hands

98.9

12

Legs

100

11

Torso

100

11

Face

39 1

11

Soles

43.2

10

Palms

34.9

11

Enlarged lymph nodes

15.6

7

Astrakhan rickettsial fever has an acute onset, the disease begins with the appearance of fever. In half of the patients, the fever is preceded by the appearance of the primary affect. In most cases, it is localized on the lower limbs, somewhat less often on the trunk and in isolated cases on the neck, head, hands, penis. The primary affect is predominantly single, occasionally two elements are observed. The formation of the primary affect is not accompanied by subjective sensations, but on the day of its appearance, slight itching and soreness are sometimes noted. The primary affect looks like a pink spot, sometimes on a raised base, from 5 to 15 mm in diameter. In the central part of the spot, a punctate erosion appears, quickly covered with a hemorrhagic dark brown crust, which is rejected on the 8-23rd day of the disease, leaving a punctate superficial atrophy of the skin. At the base of the primary affect, unlike other tick-borne rickettsioses, there is no infiltration, the skin defect is exclusively superficial in nature without deep necrotic changes in the dermis. Sometimes it is difficult to recognize among other elements of the rash.

Regional lymphadenitis is observed in every fifth patient with primary affect. The lymph nodes are no larger than a bean; they are painless, mobile, and not fused with each other.

The initial (pre-exanthematous) period of Astrakhan rickettsial fever lasts 2-6 days. It has the following symptoms of Astrakhan rickettsial fever: an increase in body temperature, reaching 39-40 ° C by the end of the day, the appearance of a feeling of heat, repeated chills, headache, joint and muscle pain. loss of appetite. The headache quickly intensifies, in some patients it becomes excruciating and deprives them of sleep. Sometimes dizziness, nausea and vomiting occur. In elderly people, fever may be preceded by prodromal phenomena in the form of increasing weakness: fatigue, fatigue, depression. The febrile reaction is accompanied by moderate tachycardia. During this period, an increase in liver is noted. Scleritis and conjunctivitis are often recorded. Hyperemia of the mucous membrane of the back wall of the pharynx, tonsils, arches and uvula of the soft palate in combination with complaints of a sore throat and nasal congestion are usually regarded as manifestations of acute respiratory infections, and in the case of coughing, as bronchitis or pneumonia.

On the 3rd-7th day of fever, a rash appears and the disease enters its peak period, which is accompanied by an increase in symptoms of intoxication.

The rash is widespread and localized on the skin of the trunk (mainly the anterolateral parts), upper (mainly on the flexor surfaces) and lower extremities, including the palms and soles. The rash is rare on the face, in cases of more severe intoxication.

The exanthema is usually polymorphic, maculopapular-roseolous-papular, hemorrhagic in nature, and in milder cases may be monomorphic. After the rash disappears, pigmentation remains. The rash on the palms and soles is papular in nature. Roseolous elements are usually abundant, occasionally single: pink or red, with a diameter of 0.5 to 3 mm. In more severe cases, fusion of roseola is observed due to their abundance. Roseola often transforms into hemorrhagic spots, most often on the lower extremities.

Most patients exhibit muffled heart sounds and tachycardia corresponding to the severity of the temperature reaction; less frequently, various rhythm disturbances (paroxysmal tachycardia, extrasystole, atrial fibrillation) are observed, and occasionally, arterial hypotension.

The tongue is coated with a grayish coating. The appetite is reduced to the point of anorexia. Cheilitis is observed. Transient diarrhea is possible in the first days of the disease. Hepatomegaly is observed in every second patient, on average until the 10th-12th day of the disease. The liver is painless, of a dense elastic consistency, its lower edge is even, the surface is smooth. Enlargement of the spleen is practically not observed.

The body temperature above 39 °C persists for 6-7 days, fever above 40 °C is rarely observed. On average, many patients are bothered by chills until the 7th day. The temperature curve is remittent, less often - constant or irregular. The febrile period lasts on average 11-12 days, ending in most cases with a shortened lysis.

The recovery period begins with the normalization of temperature. The patients' health gradually improves, the symptoms of intoxication disappear, and appetite appears. In some recovering patients, the symptoms of asthenia persist for a relatively long time.

Astrakhan rickettsial fever may be complicated by pneumonia, bronchitis, glomerulonephritis, phlebitis, metro- and rhinorrhea, infectious toxic shock, acute cerebrovascular accident. Some patients show signs of toxic damage to the central nervous system (nausea or vomiting with severe headache, bright erythema of the face, rigidity of the occipital muscles and Kernig's symptom, ataxia). No inflammatory changes are found in the examination of the cerebrospinal fluid.

The blood picture is usually uncharacteristic. Normocytosis is noted; significant changes in the formula and phagocytic activity indices are absent. In severe cases, leukocytosis, thrombocytopenia, and signs of hypocoagulation are observed. Urine testing in many cases reveals proteinuria and an increase in the number of leukocytes.

Diagnosis of Astrakhan rickettsial fever

Diagnostic criteria for Astrakhan rickettsial fever:

  • epidemiological data:
    • seasonality of the disease (April-October),
    • stay in a natural (anthropurgic) focus,
    • contact with ticks (imago, larvae, nymphs);
  • high fever;
  • severe intoxication without the development of typhoid status;
  • arthralgia and myalgia;
  • abundant polymorphic non-merging and non-itching rash on the 2nd-4th day of illness;
  • primary affect:
  • scleritis, conjunctivitis, catarrhal changes in the pharynx;
  • enlarged liver.

Specific diagnostics of Astrakhan rickettsial fever uses the RNIF reaction with a specific antigen of the pathogen. Paired blood serums taken at the height of the disease and during the recovery period are examined. The diagnosis is confirmed with a 4-fold or more increase in antibody titers. The PCR method is also used.

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Differential diagnostics of Astrakhan rickettsial fever

During the prehospital examination, diagnostic errors were made in 28% of patients with Astrakhan rickettsial fever. Astrakhan rickettsial fever should be differentiated from typhus, measles, rubella, pseudotuberculosis, meningococcemia, Crimean hemorrhagic fever (CHF), leptospirosis, enterovirus infection (enterovirus exanthema), secondary syphilis.

Differential diagnostics of Astrakhan rickettsial fever

Nosoform

Symptoms common to ARL

Differential diagnostic differences

Typhus Acute onset, fever, intoxication. CNS damage. rash, enanthema, liver enlargement. Fever is longer, up to 3 weeks, CNS damage is more severe, with disorders of consciousness, agitation, persistent insomnia, boulevard disorders, tremor: the rash appears on the 4th-6th day of illness, does not rise above the skin surface, roseolous-petechial. The face is hyperemic. The sclera and conjunctiva are injected. Chiari-Avtsyn spots: the spleen is enlarged. Primary affect is absent, lymphadenopathy. Seasonality is winter-spring, due to the development of pediculosis. Positive RNIF and RSK with Prowaczek antigen
Measles Acute onset, fever, intoxication, rash Catarrhal symptoms are expressed, rash on the 4th-5th day, erupts in stages, rough, confluent, Belsky-Filatov-Koplik spots. There is no rash on the palms and feet. There is no connection with the tick bite (contact), as well as primary CT
Rubella Fever, rash, lymphadenopathy Fever is short-term (1-3 days), there is no rash on the palms and feet, intoxication is not expressed. The posterior cervical lymph nodes are predominantly enlarged. There is no connection between the disease and the tick bite (contact), as well as the primary affect. In the blood - leukopenia and lymphocytosis

Pseudotuberculosis

Acute onset, fever, intoxication, rash

The rash is rough, more abundant in the area of the joints; symptoms of "socks", "gloves", dyspeptic syndrome. Neurotoxicosis, arthralgia, polyarthritis are not characteristic, there is no connection between the disease and the tick bite (contact), as well as the primary affect

Meningococcemia

Acute onset, fever, intoxication, rash

The rash that appears on the first day is hemorrhagic, mainly on the extremities, rarely abundant. From the 2nd day, most patients have purulent meningitis. Liver enlargement is not typical. Primary affect and lymphadenopathy are not observed. In the blood - neutrophilic leukocytosis with a shift in the formula to the left. No connection with tick bite (contact) is observed

KGL

Acute onset, fever, intoxication, rash, facial hyperemia, CNS damage, primary affect, tick bite

The rash is hemorrhagic, other manifestations of hemorrhagic syndrome, abdominal pain, dry mouth are possible. Severe leukopenia, thrombocytopenia, proteinuria, hematuria. Patients are contagious

Leptospirosis

Acute onset, chills, high fever, rash

The fever level is higher, the rash is ephemeral, not pigmented. Jaundice. Hepatosplenic syndrome. Myalgia is pronounced. kidney damage up to acute renal failure. Often - meningitis. In the blood - neutrophilic leukocytosis, in the urine - protein, leukocytes, erythrocytes, cylinders. There is no connection between the disease and the tick bite (contact), as well as the primary affect. Lymphadenopathy is absent.

Enteroviral exanthema

Acute onset, fever, intoxication, maculopapular rash, enanthem

Catarrhal symptoms are expressed. Rash on the palms and soles is rare, conjunctivitis is characteristic. enlargement of the cervical lymph nodes. Often serous meningitis. There is no connection between the disease and the tick bite (contact), as well as the primary affect

Secondary syphilis

Roseola-papular rash, lymphadenopathy

Fever and intoxication are not typical, rashes are stable, persist for 1.5-2 months, including on mucous membranes. There is no connection between the disease and tick bite (contact), as well as primary affect. Positive serological syphilitic tests (RW, etc.)

trusted-source[ 8 ], [ 9 ]

Indications for hospitalization

Indications for hospitalization:

  • high fever;
  • severe intoxication;
  • tick suction.

What do need to examine?

What tests are needed?

Treatment of Astrakhan rickettsial fever

Etiotropic treatment of Astrakhan rickettsial fever is carried out with tetracycline orally at a dose of 0.3-0.5 g four times a day or doxycycline on the first day 0.1 g twice a day, in the following days 0.1 g once. Also effective are rifampicin 0.15 g twice a day; erythromycin 0.5 g four times a day. Antibiotic therapy is carried outup to and including the 2nd day of normal calf temperature.

In case of severe hemorrhagic syndrome (profuse hemorrhagic rash, bleeding gums, nosebleeds) and thrombocytopenia, ascorbic acid + rutoside, calcium gluconate, sodium menadione, bisulfite, ascorbic acid, calcium chloride, gelatin, aminocaproic acid are prescribed.

How is Astrakhan rickettsial fever prevented?

Specific prevention of Astrakhan rickettsial fever has not been developed.

Disinfection of dogs and capture of stray dogs are important.

In epidemic foci, when staying outdoors during the season of Astrakhan rickettsial fever, it is necessary to conduct self- and mutual examinations in order to detect ticks in a timely manner. You should dress so that your outerwear is, if possible, monochromatic. This makes it easier to find insects. It is recommended to tuck trousers into golf socks. A shirt - into trousers: the cuffs of the sleeves should fit tightly to the arms. You cannot sit or lie on the ground without special protective clothing, or spend the night outdoors if safety is not guaranteed.

To protect against ticks, it is recommended to use insecticides, such as permethrin.

To reduce the risk of ticks crawling from livestock and other animals to humans, it is necessary to systematically inspect animals in the spring and summer, remove attached ticks with rubber gloves, and avoid crushing them. Ticks collected from animals should be burned.

A tick that has attached itself to a person must be removed with tweezers along with its head; the bite site must be treated with a disinfectant solution; the tick must be sent to the State Sanitary and Epidemiological Surveillance Center to determine whether it is infectious.

What is the prognosis for Astrakhan rickettsial fever?

Astrakhan rickettsial fever has a favorable prognosis.

Patients are discharged 8-12 days after normalization of body temperature.

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