This acute infectious disease occurs when bitten by an infected pasture tick or other infected animals. Typhus is accompanied by fever, signs of general intoxication of the body and the appearance of a maculopapular rash. Now the disease does not occur in developed countries; it more often affects people in Africa and Asia.

Symptoms of tick-borne typhus

Like any other disease, the development of this disease occurs in several stages.

Incubation period

It lasts from three to five days and is accompanied by the following symptoms:

• high temperature reaching 40 degrees;
• fever followed by chills;
• thirst;
• visual, tactile and auditory hyperesthesia;
• vomit.

Acute stage of the disease

The fever lasts for a week and a half, and in the last three days there is a decrease in temperature.

During the entire period of fever, the patient is concerned about the following signs of typhus:

• headache and muscle weakness, which is concentrated in the lumbar region;
• slow pulse;
• increase in the size of the spleen;
• drop in blood pressure;
• hyperemia of the facial skin and redness of the eyes.

As typhus progresses, the following symptoms occur:

1. On the area of ​​skin affected by the bite, a primary affect appears, expressed by a dense, small infiltrate with a brown-black crust. This formation is also accompanied by the formation of lymphadenitis, characterized by enlarged lymph nodes.
2. Rashes are found on the back, chest, flexion areas of the limbs, feet and palms. The rash persists throughout the feverish state and often after the illness skin pigmentation forms in its place.
3. In severe situations, typhoid status develops, which is accompanied by mental disorder, talkativeness, excessive mental arousal and memory impairment. Shallow sleep with terrible dreams leads to the fact that patients are simply afraid to sleep.

Recovery

As you recover, the signs of typhus begin to recede. This period is characterized by a decrease in the rash. However, for another two weeks the patient is bothered by apathy, weakness, and pale skin.

Complications of tick-borne typhus

The disease can provoke the following serious consequences:

• infectious-toxic shock, accompanied by a decrease in temperature due to heart failure;
• the disease may result in thromboembolism, myocarditis and thrombosis;
• damage to the nervous system (meningitis);
• in the event of a secondary infection, pneumonia and furunculosis begin to develop;
• Bed rest can cause bedsores.

Treatment of typhus

Patients suffering from typhus must take antibiotics that inhibit the activity of the pathogen. Such drugs include Levomycetin and Tetracycline, which are taken for a course of at least ten days.

Also an important component of treatment is taking antipyretics (Ibuprofen, Paracetamol), glycosides (Strophatin). As a rule, the patient is prescribed infusion therapy, which involves the use of crystalloid and colloid compositions.

General description

Ixodid ticks have a well-developed proboscis and body with several pairs of legs. Before feeding begins, their sizes do not exceed a couple of millimeters - for females - 3-4 mm, for males - no more than 2.5 mm. But after saturation, their volumes increase tenfold.

But if a person enters their natural habitat, then they attack people.

Routes of infection

After an ixodid tick bite, many different pathogens of dangerous diseases enter the host’s circulatory system. Having reached an open area of ​​skin, the ticks bite firmly into their feeder in less than an hour.

In this case, all its oral organs, together with the head, are under the skin. It is securely attached thanks to saliva with a special composition. As a result, the tick can remain on the body from several hours to several days.

Ixodid ticks are sometimes called encephalitic, as they are carriers of such dangerous diseases as tick-borne encephalitis, Crimean hemorrhagic fever, borreliosis, anaplasmosis, etc.

In the first hours after the bite, symptoms are characterized by the appearance of weakness, drowsiness, chills and aching joints. The more ticks there are on the body, the more intense the above symptoms will be. People with allergies will experience more severe symptoms.

Among the first symptoms are: redness; increased body temperature (37-38°C); decrease in pressure; tachycardia - an increase in heart rate to more than 60 per minute; the appearance of rash and itching; enlarged lymph nodes in the area of ​​the bite. In addition, severe headaches, nausea and vomiting, difficulty breathing, hallucinations, etc. may appear.

Elevated temperature is of particular importance, since fever that appears within 2-10 days after a tick bite can signal an infectious infection.

Drug treatment

The most effective measure against infection by infections carried by ixodid ticks is preventive vaccination, which is carried out a month before the ticks become active. In the absence of vaccination, an effective protective measure is urgent vaccination with immunoglobulin.

Not every bite leads to the development of disease. But if you are bitten by a tick, remove it, store it in some container and take it to a laboratory to determine whether it was contagious.

If the answer is yes, start treatment immediately! Infection can be avoided if the insect is removed correctly (completely) immediately.

Treatment with folk remedies

• Place the onion pulp on a piece of clean cloth or gauze and bandage it to the wound;
• It is recommended to put natural royal jelly under the tongue an hour before meals; you can mix it with honey;
• To relieve redness and swelling, use an infusion of green walnuts. Grind the fruits, place them in a jar and fill them with vodka, leaving them for a month. Take a small spoon three times a day before meals;
• Three times a day you should take 15-20 drops of Rhodiola rosea (golden root) tincture, diluted in a small amount of warm water. You can mix Rhodiola rosea root with wormwood in equal proportions. The mixture should be infused with alcohol and taken 25-40 drops, also diluted with a small portion of water.

oriental fluke lanceolate fluke liver fluke Siberian fluke pinworms roundworms head lice lamblia Siberian fluke cat fluke blood flukes bovine and pork tapeworms

General description

There are three types of lice:

• Cephalic - live on the scalp;
• Pubic - live in the groin area, can also live in the armpits and eyebrows;
• Clothes - live in the folds of a person's clothing, only sometimes crawling onto the wearer's body to feed on his blood.

These types of lice give rise to three corresponding types of lice: pubic, head and body lice. There is also a possibility that these varieties form a mixed type of pediculosis, that is, with combined symptoms of each subspecies of pediculosis.

They reproduce by laying eggs called nits. They are attached to the hairs closer to the skin using an adhesive substance and are oval in shape (dimensions 0.8 x 0.3 mm). The female lays an average of 10 eggs per day. The period of development of an egg into an adult takes 12 days. If no measures are taken, the reproduction cycle is repeated every 3 weeks.

Lice use their mouthparts to pierce the skin of their host, suck out their blood and lay their eggs (nits). The most common head lice are those that live on the scalp. Head lice live on average 3 weeks, outside their habitat they will live a maximum of 1 week, nits a little more - 2 weeks.

Lice feed on blood, which they suck from the scalp. A person may feel itching after 2-4 weeks. This is because after piercing the skin, the head louse releases its saliva into the wound.

Routes of infection

The appearance of head lice in humans is not always associated with poor personal hygiene. These insects can crawl from one head to another upon close contact.

Pediculosis is particularly widespread in kindergartens, schools, boarding schools, and other public places. Infection can also occur in transport, as well as when using the personal items of an infected person, his comb, towel, hairpin or hat.

Lice feed on blood, causing scalp irritation and itching - these are the first symptoms of lice. By scratching the bite site, you can introduce infection into the wounds, which can be a complication of lice. The skin becomes inflamed, redness appears, and body temperature may rise.

Drug treatment

The following medications are used to treat lice:

• "Nittifor" - liquid solution or cream;
• “Medifox”, “Medifox-super” – gel, emulsion;
• “Pair Plus” - aerosol;
• "Nix" - cream;
• "Permethrin ointment";
• “Pedex” – lotion, gel;
• “Nittifor – solution, cream;
• "Pedilin" - shampoo;
• “Nok” – shampoo;
• "Higia" - shampoo.

After treating the head according to the instructions, the hair must be thoroughly combed with a fine comb with a roller strung on it, and after 3 weeks the treatment must be repeated, since during this time new lice may appear from the remaining nits.

General description

There are about 2,000 species of fleas in nature. These blood-sucking insects feed on the blood of mammals. Their scientific name Siphonaptera translates from Greek as “wingless pump”, as they feed on the blood of mammals.

The size of fleas is 2-8 mm in length, their body is laterally compressed, and there are three pairs of legs on the chest. The last pair of legs are greatly enlarged, giving them their fantastic jumping ability. There are no wings.

Color ranges from light to dark brown. Thanks to the presence of a kind of sensory organ, they are able to detect air vibrations, heat, vibration, and the presence of carbon dioxide, which indicates the presence of a potential food source nearby - an animal or a person. However, fleas can go several months without food.

Fleas carry pathogens of a number of dangerous diseases:

• Pseudotuberculous mycobacterium;
• Pasteurellosis;
• Tularemia;
• Bubonic plague;
• Intestinal yersiniosis;
• Salmonellosis;
• Brucellosis;
• Epidemic typhus;
• Helminthiases;
• Hepatitis B, C, etc.

The Japanese in 1942-1945 used fleas as carriers of bacteriological weapons, with the help of which more than 400 thousand people were killed.

Routes of infection

Fleas are brought indoors by pets, rats, mice, where they fall from dirt and leaves lying on the ground.

Fleas can also migrate from neighboring infested premises, from building basements and entrances.

A warm and humid habitat is ideal for them. Cold temperatures slow down their life cycle, so summer is the ideal time for them to reproduce and develop.

In the house, fleas live in cracks and cracks in the floor, joints between walls and floors, carpets, rugs, and under baseboards. If there are animals indoors, fleas concentrate in the area of ​​their bedding, sleeping baskets and furniture. Adults live directly on their food source - domestic animals.

Externally, flea bites are similar in many ways to mosquito bites, but they take much longer to heal. Within half an hour, the bite site swells, turns red and itches very much. After one or two days, the area turns into a small wound or abscess and may even bleed.

When a flea bites, they inject saliva into the wound, which contains an analgesic, which prevents the bite from being immediately detected, but later causes irritation and itching.

Drug treatment

Fleas are resistant to most insecticides, but preparations containing fipronil, fluvalinate, cypermethrin, and cyfluthrin are effective against them.

Also, to combat fleas, insecticidal preparations based on FOS (chlorophos, karbofos, fenthion), carbamate (propoxur), pyrethroids (permethrin, deltamethrin, cypermethrin, fenvalerate, cyphenothrin), neonicotinoids, etc. are used.

Treatment with folk remedies

You can get rid of fleas in an apartment using salt and soda, which is sprinkled on carpets and floor coverings, and then vacuumed, after which the vacuum cleaner must be thoroughly cleaned.

Fleas cannot tolerate certain odors: wormwood, pine needles, mint, eucalyptus, tobacco, tansy, garlic. Bunches of plants can be placed in potential flea habitats and they will go away.

General description

Science knows more than 30 thousand types of bedbugs, but the most common in houses and apartments are bed bugs, which are also called sofa and linen bugs.

The lifespan of a bed bug is 1 year. During the year of her life, the female lays up to 500 eggs. The full development cycle of a bedbug is 40 days from egg laying. If bedbugs do not have enough food or at low temperatures they go into suspended animation.

Bedbugs crawl out at night to hunt (a bug feeds on human blood every 5-10 days, and drinks twice its own weight), bedbugs are especially active from 2 a.m. to 6 a.m.

During the day they hide in carpets, blankets, pillows, mattresses, upholstered furniture, climb into household appliances, into cracks in walls, under wallpaper. They find shelter in dark and warm places. They love to live in pillows and mattresses on which cats and dogs sleep, and in the cages of other pets.

Routes of infection

The appearance of bedbugs at home has nothing to do with the sanitary condition of the home. After all, the source of food for them, unlike cockroaches, house ants, and kitchen moths, is not food supplies, but the person himself.

Bedbugs can enter indoors through doors, windows and vents in apartment buildings. They can come with you from hotels, old houses, transport, where you spent the night; They can even nest in newly purchased furniture and mattresses.

Bedbugs can be brought in by visiting guests or unscrupulous workers living in areas infested with bedbugs.

Bed bugs can cause a severe allergic reaction that includes itching, blistering, severe swelling and redness. Sometimes, when scratching, due to the addition of a secondary infection (especially if the immune system is weakened), pustules and inflammations can form, leaving scars on the skin.

In rare cases, large numbers of bedbug bites can cause iron deficiency anemia in children.

Drug treatment

When starting the fight against bedbugs, it is important to remember that they have the ability to spread very quickly. Therefore, if you live in an apartment building, then you need to fight together with your neighbors. The most reliable way is to call a pest control service, but to do this you will have to leave your home for several days.

Today, there are powerful chemical agents for independent control of bedbugs in an apartment: “Delta Zone”, “Executioner” (Germany), “Klopomor” (Russia), “Kombat” (Korea), “Karbofos” (Russia), etc.

We should not forget that the more effective the product, the more toxic it is, so you must strictly follow the instructions and observe safety precautions, and during massive treatment, leave the apartment for several days, taking your pets.

Treatment with folk remedies

• Using a steamer or steam generator, go over the furniture upholstery and all the places where “traces” of bedbugs were found. Bedbugs die at a temperature of 50°C;
• Freezing: extremely low temperature for bedbugs - below -20ºС. Therefore, in severe frost, you can take out a sofa, mattress, etc. in the cold so that the bedbugs die. The room also needs to be frozen out, leaving the windows open for several days.

To quickly remove bedbugs at home, the following emulsion recipes will be useful:

• Mix 100 ml of kerosene and turpentine. Add 20 g of naphthalene to the resulting solution;
• Pour 3 g of salicylic acid into a container, pour 20 g of phenol and add 40 g of turpentine;
• Mix 10 ml of turpentine in 100 ml of water. To obtain a caustic emulsion, add 15 ml of kerosene and about 30 g of green soap;
• Combine 10 g of ammonia, 40 g of benzene and 150 g of denatured alcohol.

The prepared solutions act upon direct contact with bedbugs and eggs. Therefore, to destroy the population, it is necessary to pour the emulsion directly onto the pests and their habitat.

General description

Fungal diseases, medically called mycoses, have become widespread in our time.

Fungal diseases of the body belong to superficial mycoses, among which are:

• Keratomycosis is a fungal infection of the upper layer of skin. This group includes pityriasis versicolor, nodular trichosporia, erythrasma, axillary trichomycosis;
• Dermatomycoses are deeper lesions of the skin caused by dermatophytes, yeast or mold fungi. Among them are epidermomycosis, microsporia, rubromycosis, trichophytosis, favus;
• Candidiasis is a pathological lesion of the skin and mucous membranes by yeast-like fungi Candida albicans; distinguish urogenital, oral candidiasis, skin and nail candidiasis, internal organ candidiasis;

Routes of infection

Keratomycosis is characterized by the localization of fungi in the stratum corneum of the epidermis without affecting the skin appendages, in the form of light brown spots, sometimes with a pinkish tint, with noticeable pityriasis-like peeling, most often on the neck, back, chest and shoulders. There are no inflammatory reactions of the skin during the period of exacerbation, as well as feelings of discomfort.

Dermatomycosis is characterized by the following symptoms: red round spots on the skin; skin diaper rash, peeling; deformation, change in nail structure; changes in the area of ​​interdigital folds; itching in the affected area.

Candidiasis causes different symptoms depending on the location.

Drug treatment

Fungus on the body should be treated comprehensively. In order for a doctor to prescribe adequate therapy, it is necessary to undergo a study to determine the type of microorganism. Fungal treatment includes:

• Local use of antimycotics (Mikozolon, Mikoseptin, Mikospor, Mikozoral, Nizoral, Kanizon, Mikozan, Mifungar, Lamisil, Mikoterbin, Candide, Triderm, Ekalin, etc.);
• Systemic administration of antimycotics with fluconazole, itraconazole, miconazole, ketoconazole, clotrimazole, econazole or other imidazole and triazole derivatives (Diflucan, Forcan, Mikosist, Nizoral, Flucostat, etc.);
• The use of antifungal antibiotics of the polyene series (nystatin, natamycin, amphotericin, levorin);
• Use of glucocorticosteroid drugs;
• Taking antihistamines, immunomodulators and multivitamins.
• Physiotherapeutic procedures (medicinal electrophoresis, pulsed magnetic therapy, UHF therapy).

Treatment with folk remedies

• Coffee baths can combat fungus on the hands, feet and body (only natural coffee, not instant!);
• An ointment made from butter with chopped garlic is applied to the affected areas of the body;
• Wipe the affected areas on the body twice a day with a 20% alcohol solution of propolis;
• Do the same with onion juice for 3-5 days;
• Onion, ground into a paste, is placed between the fingers for 30 minutes, after which the feet are washed in warm water;
• Lubricate the affected skin with alcohol tincture of garlic;
• Rub lemon into folds of skin twice a day for a week.

General description

The microscopic subcutaneous demodex mite is found in 90% of the population during research, but only in rare cases causes skin diseases: in people with a weakened immune system, metabolic disorders, in the elderly and in children with pathologies of the gastrointestinal tract.

Demodex includes many types of mites. Its two main types include:

• Demodex brevis. This type of mite living under the skin lives and reproduces in the ducts of the sebaceous glands. It has a short body of about 0.15 mm.
• The human mite Demodex folliculorum is localized in hair follicles and has a long, elongated body up to 0.45 mm.

It feeds on the secretion of the sebaceous glands or dead skin cells. Absorbs all nutrients from hair roots. The life cycle of a demodex mite is about two to three weeks, after which the individual dies and the decay products begin to poison the body.

Routes of infection

It is believed that the disease begins to manifest itself after stress and emotional stress, when the immune system weakens.

The disease begins with the appearance of acne and irritation, peeling of the skin, and redness. The following symptoms are noted:

• The skin is lumpy, with an earthy-gray tint, small hard calcified lumps form in the thickness of the skin;
• Enlarged pores and increased sebum secretion, areas of affected skin look moist, with a characteristic oily sheen;
• A lot of acne appears, including purulent ones, weeping sores, rashes, red spots, then acne appears on the chest, back and even thighs;
• Sometimes there is an unbearable itching that gets worse at night, or a slight tickling sensation, as if someone is crawling on the skin;
• Itching in the eyelids and scalp, increased loss of eyelashes and hair;
• Itching in the ears and ear canals;
• The nose increases in size, sometimes significantly, and facial movements are difficult.

Drug treatment

At the acute stage, antibiotics are prescribed to relieve inflammatory processes, sedatives, except antidepressants. Immunocorrective therapy is carried out. Treatment of demodicosis is complex.

Treatment of demodex with electrophoresis with moisturizing substances and a course of microdermabrasion have worked well.

👉Expert opinion about the drug.

General characteristics .

Under natural conditions, rickettsiosis is observed in blood-sucking arthropods, in a number of wild (rodents and small animals) and domestic animals (small and cattle, dogs), as well as in humans.

In arthropods and vertebrates, rickettsiosis usually occurs as a latent infection, but lethal forms are also observed. In humans, rickettsiosis, as a rule, occurs in the form of an acute febrile illness with the development of multiple vasculitis and thrombovasculitis of small vessels of various systems and organs, often with damage to the central nervous system and a characteristic hemorrhagic exanthema. Latent forms of rickettsial infection, detected serologically, are also observed.

All zoonotic rickettsioses are typical natural focal infections, the nosoarea of ​​which is determined by environmental factors, the spread of sensitive animals and blood-sucking arthropods. Enzootic foci of rickettsiosis can acquire epidemiological significance if non-immune individuals enter their territory and become infected through the bites of infected blood-sucking arthropods or through contact with contaminated material.

Rickettsial diseases are widespread. Some of them are found everywhere, for example Q fever, others are observed in those countries where landscape and climatic conditions contributed to the formation and maintenance of natural foci of these infections. They have become widespread in countries with hot climates.

Diagnosis of rickettsial diseases is based on a complex of epidemiological and clinical data. Serological research methods - RSK, RPGA, rickettsia agglutination reaction (RAR), RIF - are of great importance in recognizing rickettsial infections and identifying abortive and latent forms of infection.

Tick-borne typhus of North Asia

Definition .

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

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

Historical information .

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

Etiology and epidemiology .

Causative agent of tick-borne rickettsiosis RickettsiaSibirica belongs to the genus Rickettsia, family Rickettsiaceae, is similar to other rickettsiae, multiplies in the cytoplasm and nucleus of affected cells.

In foci of the disease, circulation of the pathogen occurs between wild mammals and ixodid ticks ( Dermacentor, Haemaphysalis, Ixodes) – natural and main reservoirs R. sibirica. In ticks, transovarian and transphase routes of transmission of rickettsiae are observed. Human infection 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, which is due to the period of greatest activity of ticks. In autumn, a second rise in incidence is possible, determined by the second generation of arthropods. Sporadic diseases occur mainly among agricultural workers. The range of tick-borne 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.

.

At the site of the entrance gate of infection, a primary affect occurs - an inflammatory reaction of the skin with regional lymphadenitis. The pathogen invades the endothelium of small vessels, causing inflammatory changes in them. In this case, proliferative processes prevail over destructive ones with the development of endoperivasculitis, which explains the milder course of the disease compared to epidemic typhus. Rickettsemia and toxinemia in tick-borne rickettsiosis cause symptoms of intoxication of the body.

Clinical picture .

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 a prodromal period in the form of malaise, headaches, muscle pain, and loss of appetite. Hyperemia of the face, neck, mucous membrane of the pharynx, as well as enanthema are often observed.

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

The leading symptoms in the clinical picture of the disease are symptoms of damage to the nervous system in the form of persistent, sometimes painful headaches, muscle and lower back pain. Unlike epidemic typhus, tick-borne typhus statustypephosus absent. Occasionally, meningeal symptoms are detected. Conjunctivitis and scleritis, bradycardia and hypotension are noted.

A constant symptom is a rash that appears on the 2-5th day of illness. In most patients, it appears first on the trunk, and then spreads to the limbs, where it is localized mainly on the extensor surface and in the circumference of the joints. With a profuse rash, elements of the rash can be on the face, palms, and soles. The rash is characterized by polymorphism and is predominantly roseola-papular in nature. A more severe course of the disease is accompanied by hemorrhagic rashes. After a few days, the rash gradually fades away, remaining longest in the area of ​​the lower extremities and buttocks in convalescents; Brownish pigmentation persists for a long time at the site of individual elements of the rash.

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

.

Specific diagnostics involve isolating a pure culture R. sibirica from the blood of a patient using guinea pigs (scrotal reaction). Serological diagnosis is carried out using RSC using 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, which is 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.

Marseille fever

Definition .

Synonyms: Mediterranean tick fever, pimple fever, Carducci-Olmer disease, summer typhus.

Marseilles fever ( Ixodorickettsiosismarseliensis, Febrismediterranes) is an acute transmissible zoonotic rickettsiosis. It is characterized by a benign course, moderately expressed generalized vasculitis, manifested by an acute febrile state, the presence of primary affect and widespread maculopapular exanthema.

Historical information .

The disease was first described Conor, Bruck in Tunisia in 1910 under the name "pimple fever". A similar clinic was described in the study of the so-called canine disease D. Olmer And J. Olmer in Marseille in 1928, after which the term “Marseille fever” was established in the literature. In 1930 Durand, Conseil in Tunisia they proved the role of the dog tick Rhipicephalussanguineus in the transmission of infection, and Blanc, Caminopetros(1932) established transovarial transmission of the pathogen in ticks.

The causative agent of Marseilles fever was isolated Caminopetros(1932), but described in detail Brumpt (1932).

Etiology .

The causative agent of Marseille fever - Dermacentroxenus conori - has all the properties inherent in rickettsia of the subgenus Dermacentroxenus. It multiplies in the cytoplasm and nucleus of affected cells. Immunological similarity noted D. conori with pathogens of rocky mountain spotted fever and North Australian tick-borne typhus. Geographic strains described D. conori, causing diseases similar to Marseilles fever.

Epidemiology .

Man is a random link in the chain of circulation D. conori. He becomes infected with Marseilles fever after being attacked and bitten Rh. Sanguineus, when crushing well-fed ticks on the skin, less often - when introducing infected tissues of vectors onto the mucous membranes. People's sensitivity to D. conori relatively low in all age groups.

The incidence is sporadic; there are no epidemiological outbreaks. Transmission of the infection in the tropics occurs throughout the year; in temperate regions, there is a summer peak in incidence associated with maximum vector activity.

Marseilles fever is common mainly in countries with warm and hot climates. It is registered in the Mediterranean Sea basin (in Portugal, Spain, southern France, Italy, Morocco, Tunisia, Algeria, Tripoli, the Arab Republic of Egypt), in Russia in the coastal regions of the Caspian and Black Seas, in Africa and India.

Pathogenesis and pathological anatomy .

Rickettsiae that enter the human body through the skin or mucous membranes multiply in reticuloendothelial cells and, after their destruction, enter the blood, causing specific endotoxemia. At the site of rickettsia introduction, a characteristic inflammatory-proliferative infiltrate develops, followed by necrosis and ulceration - primary affect (“black spot”).

Rickettsia endotoxins cause functional and morphological changes in the nervous, cardiovascular, endocrine and other systems. In the vessels, proliferation of the endothelium and widespread infiltration with lymphocytes, monocytes, and, less often, polynuclear cells are observed, later on – endoperivasculitis. Lesions of skin vessels appear in the form of a characteristic exanthema.

Clinical picture .

Marseilles fever is a benign disease. The incubation period lasts from 3 to 7 (sometimes up to 18) days. The onset of the disease is acute: short-term chills appear, the temperature quickly rises to 39–40 oC, headache, general weakness, insomnia, pain in the muscles and lumbar region are noted. In rare cases, a short-term disorder of consciousness and a meningeal symptom complex are possible. General toxic manifestations are observed throughout the febrile period, the duration of which ranges from 10–14 to 22 days. Fever is usually remitting.

When examining patients in the first days of illness, facial hyperemia and scleral injection are noted; in most of them, primary affect is detected at the site of rickettsia introduction. The primary affect is located at the site of a tick bite on the skin of closed areas of the body, especially on the lower extremities, and is a small ulcer with a diameter of 2–5 mm on a hyperemic infiltrated base, with a dark scab in the center. Sometimes 2–3 primary affects can be identified. The scab persists throughout the febrile period and disappears on the 4-5th day of apyrexia with the formation of a delicate, sometimes pigmented scar.

In cases of rickettsia introduction through the mucous membranes of the eye, conjunctivitis or keratoconjunctivitis develops, accompanied by chemosis.

Regional lymph nodes are somewhat enlarged and painful. The reverse development of lymphadenitis occurs towards the beginning of recovery.

From the 2-3rd day of the disease, an abundant large roseolous or maculopapular rash appears on the skin of the face, trunk and extremities, including the palmar and plantar surfaces, which after 2-3 days turns into papular-petechial exanthema with papules ranging in size from 5 to 10 mm. The rash persists until the end of the febrile period and gradually disappears during the period of apyrexia, pigmentation remains for 2-3 weeks (less often than months).

Impairments in the function of the cardiovascular system are usually moderate and are detected in the form of bradycardia. In some cases, tremor of the tongue, limbs, delirium and meningism are noted.

Splenomegaly is observed inconsistently; the liver is rarely enlarged. In the blood, leukopenia with relative lymphocytosis is more common. ESR is increased.

As a rule, Marseilles fever does not cause complications and ends with recovery.

Diagnosis and differential diagnosis .

The diagnosis is established on the basis of epidemiological, clinical and laboratory data.

It is important to detect primary affect, regional lymphadenitis, and widespread maculopapular exanthema. This triad distinguishes Marseilles fever from other diseases that occur with exanthemas.

Specific diagnosis consists of isolating a culture of rickettsia during intraperitoneal infection of guinea pigs and serological studies (RSC and RPGA with purified antigen D. conori).

It is necessary to differentiate Marseilles fever from other rickettsioses, typhoid and paratyphoid diseases, hemorrhagic fevers, and drug-induced dermatitis.

Treatment and prevention .

The basis of treatment is the use of antibacterial drugs with anti-rickettsial activity. These include tetracyclines, macrolides, rifampicin, fluoroquinolone, chloramphenicol. Tetracycline is prescribed 0.3 g 4 times a day, doxycycline - 0.2 g for the first dose, then 0.1 g twice a day. Erythromycin, sumamed, rulid are used in the treatment of pregnant women and children according to the usual regimens. Rifampicin is prescribed at 0.3 g per day, fluoroquinolone - in medium therapeutic doses twice a day, chloramphenicol - 0.5 g 4 times a day. Antibiotics are taken until the 2-3rd day of normal temperature. In cases of hemorrhagic manifestations, calcium supplements and Vicasol are indicated. In more severe cases, corticosteroids are prescribed, and, if necessary, analgesics, antipyretics, and sedatives.

Anti-epidemic measures in hotbeds of Marseilles fever come down mainly to the destruction of ticks Rh. Sanguineus using acaricidal agents. Veterinary supervision of dogs is of great importance, examining them at least 2 times a year and destroying stray animals. Personal prevention involves using repellents.

Smallpox (vesicular) rickettsiosis

Definition .

Synonyms: gamasic rickettsiosis, rickettsial smallpox. Smallpox rickettsiosis is a benign vector-borne rickettsial infection. It is characterized by specific intoxication, moderate fever, the presence of primary affect and specific papular-vesicular exanthema.

Historical information .

The disease was first described in 1946–1947. in the outskirts of New York and due to its similarity with chickenpox, it was called rickettsial pox ( rickettsialpox). In the 50s In the 20th century, the disease was identified in other areas of the United States, in Central and Southern Africa, in Uzbekistan, Turkmenistan and Kazakhstan.

Etiology and epidemiology .

The causative agent of smallpox rickettsiosis is RickettsiaakariHuebneretal, 1946, belonging to the subgenus Dermacentroxenus. In its properties, the pathogen is close to other rickettsia from the group of tick-borne spotted fevers.

A person becomes infected with smallpox rickettsiosis in epizootic foci as a result of attack and sucking of infected gamas ticks.

Diseases in the form of sporadic cases are observed in urban and rural areas throughout the year, with an increase in the incidence rate during the period of tick activity (May-August). Men get sick more often.

Smallpox rickettsiosis is known in North America, Central and South Africa, and in the southern regions of Ukraine.

Pathogenesis and pathological anatomy .

Rickettsia, having entered the human body through a tick bite, multiply in reticuloendothelial cells, destroy them and enter the blood, causing specific endotoxemia and morphological changes in the vessels of various organs. At the site of rickettsia introduction, an inflammatory reaction with lymphangitis and regional lymphadenitis develops - the primary affect.

Vascular lesions consist of perivascular infiltration by lymphocytes and endothelial proliferation. Vascular disorders underlie the development of exanthema.

Clinical picture .

The duration of the incubation period for smallpox rickettsiosis has not been precisely established and is apparently about 7-10 days.

Even during the incubation period (5–7 days before the development of intoxication syndrome), an inflammatory infiltrate 1–2 cm in size in the form of a red papule appears on the skin at the site of the tick bite. Then the papule turns into a vesicle that penetrates deeply into the skin, and when it shrinks and dries, a black scab is formed. The primary affect is usually located on closed parts of the body, but can be noted on the back of the hands, neck, face and is combined with regional lymphadenitis. Primary affect lasts 3–3 1/2 weeks; Once it heals, a delicate scar remains.

5–7 days after the onset of the primary affect, patients acutely develop intoxication syndrome, experiencing high fever (39–4 °C), chills, severe headaches, insomnia, muscle and back pain. A remitting fever persists at high levels for 6–7 days and ends with a critical or crysolytic decrease in temperature. From 2–3 days of the febrile period, a macular-papular or erythematous rash appears.

After 1–2 days, the rash becomes vesicular with a diameter of elements up to 2-10 mm or more. The rash spreads over the entire body, including the face and sometimes also the palms and soles. The elements of the rash are not abundant and can be easily counted. In rare cases, elements of the rash may not turn into vesicles or simulate erythema nodosum. Subsequently, the vesicles dry out, and in their place black crusts form, falling off on the 4-10th day of illness without scar formation.

Signs of damage to the cardiovascular system and internal organs are usually minor.

The hemogram can reveal slight leukopenia, neutropenia with a shift in the leukocyte formula to the left, and thrombocytopenia. ESR is moderately increased.

The disease proceeds without complications and ends with recovery.

Diagnosis and differential diagnosis .

Clinical diagnosis is based on a complex of epidemiological and clinical data, of which the most important is the detection of primary affect with the subsequent development of fever and vesicular exanthema.

Laboratory diagnosis is confirmed by isolating a culture of rickettsia (on a chicken embryo, when infecting guinea pigs), as well as by using serological methods (RSC with soluble antigen R. akari). Due to antigenic affinity R. akari with other representatives of the subgenus Dermacentroxenus serological reactions are carried out in parallel with several antigens.

Differential diagnosis of smallpox rickettsiosis is carried out in relation to other tick-borne spotted fevers and chickenpox.

Treatment and prevention .

Etiotropic drugs are used, including tetracycline derivatives or chloramphenicol in normal dosages, throughout the febrile period and the first week of apprexia. Measures are also taken to prevent secondary infection.

South African tick fever

Definition .

South African tick fever is a vector-borne tick-borne zoonotic rickettsiosis. It occurs in the form of typhus-like fever with the presence of a primary affect and often a roseolous-papular rash.

Historical information .

The history of the disease was first described in Angola in 1911. Sant'Anna And Mcў Naught (tick-bitefever). The causative agent of the disease is isolated and described Pinkerton in 1942

Etiology and epidemiology .

The causative agent of South African tick fever is D. rickettsi var. Pijperi Pinkerton, 1942, similar to D. conori, however, convalescents exhibit homologous immunity with preserved susceptibility to infection D. conori.

As with other diseases from the group of tick-borne spotted fever, the natural reservoir of rickettsia is ixodid ticks Amblyommahebraum, haemaphysalisleachi and others.

A person becomes infected in foci of rickettsiosis, being attacked by infected ticks. The disease usually occurs in sporadic cases during the hot season in Angola and eastern South Africa (from Cape Kay to Kenya).

Pathogenesis and pathological anatomy .

The pathogenesis and pathological anatomy of this rickettsiosis are similar to those of Marseilles fever.

Clinical picture .

The clinical manifestations of South African tick fever vary depending on the severity of the disease and are very similar to the clinic of Marseille fever. The incubation period lasts about a week. In severe and moderate cases of the disease, the initial period develops acutely, with tremendous chills, an increase in temperature up to 4 ° C, intense headache, insomnia, possible confusion, photophobia and meningeal symptom complex. High fever persists for 10–12 days.

When examining patients in the first days of the disease, one can detect a primary affect corresponding to the site of the tick bite, in the form of a painless red infiltrate measuring 2–5 cm, with central dark necrosis and regional lymphadenitis. On the 5-6th day, a characteristic roseola rash appears, soon turning into a maculous-papular purplish-red exanthema. Elements of the rash spread throughout the body, often affecting the palmar and plantar surfaces. As the temperature decreases, the rash disappears, leaving pigmentation.

Mild forms of the disease are characterized by short-term fever, mild manifestations of intoxication, the presence of primary affect, and a scanty papular rash on the trunk and upper extremities. In some cases there is no rash. The prognosis is favorable for all forms of the disease.

Diagnostics .

Clinical diagnosis of the disease is based on epidemiological data and the results of a clinical examination of the patient. It is difficult to differentiate South African tick fever from Marseilles fever due to the great similarity of both diseases. There is an assumption that South African fever is a variant of Marseilles fever.

Specific diagnosis is carried out using infection of guinea pigs and serological methods (RSC).

Treatment and prevention .

Treatment and prevention are identical to those for other vector-borne tick-borne rickettsioses.

NORTH ASIA (RICKETSIOSIS SIBIRICA,
IXODORICKETTSIOSIS ASIATICA)
Synonyms: tick-borne rickettsiosis, tick-borne rickettsiosis of Siberia, coastal tick-borne rickettsiosis, Siberian tick-borne typhus, Far Eastern tick-borne fever, eastern typhus; sibirian tick typhus, tick-borne rickettsiosis of North Asia - English.
Tick-borne typhus of North Asia is an acute rickettsial disease characterized by a benign course, the presence of primary affect, regional lymphadenitis and a polymorphic rash.
Etiology. Pathogen - Rickettsia sibirica was opened in 1938. O.S. Korshunova. Like other pathogens of the group of spotted fevers, it parasitizes both in the cytoplasm and in the nucleus of the affected cells. Antigenically it differs from other rickettsiae in this group. Contains a toxic substance. Characterized by properties common to all rickettsiae. Able to persist for a long time in the external environment at low temperatures (up to 3 years). Keeps well when dried. The virulence of individual strains varies significantly.
Epidemiology. The disease is classified as a zoonotic disease with natural focality. Natural foci have been identified in the Primorsky, Khabarovsk and Krasnoyarsk territories, in a number of regions of Siberia (Novosibirsk, Chita, Irkutsk, etc.), as well as in Kazakhstan, Turkmenistan, Armenia, Mongolia. The reservoir of rickettsia in nature is about 30 species of various rodents (mice, hamsters, chipmunks, gophers, etc.). Transmission of infection from rodent to rodent is carried out by ixodid ticks (Dermacentor nuttalli, D. silvarum, etc.). The infestation of ticks in foci reaches 20% or more. The incidence in the tick habitat ranges from 71.3 to 317 per 100,000 population per year. The immune layer of the population in natural foci ranges from 30 to 70%. Rickettsia remain in ticks for a long time (up to 5 years); transovarial transmission of rickettsia occurs. Not only adult ticks, but also nymphs participate in the transmission of infection to humans. Rickettsia is transmitted from ticks to rodents through blood sucking. A person becomes infected during his stay in the natural habitats of ticks (shrubs, meadows, etc.), when he is attacked by infected ticks. The greatest activity of ticks is observed in spring and summer (May-June), which determines the seasonality of the incidence. The incidence is sporadic and occurs mainly among adults. Not only rural residents get sick, but also those traveling outside the city (garden plots, recreation, fishing, etc.). In recent years, about 1,500 tick-borne rickettsiosis diseases are registered annually in Russia.
Pathogenesis. The portal of infection is the skin at the site of the tick bite (rarely, infection occurs when rickettsia is rubbed into the skin or conjunctiva). At the site of introduction, a primary affect is formed, then the rickettsiae move along the lymphatic pathways, causing the development of lymphangitis and regional lymphadenitis. Lymphogenously, rickettsiae penetrate into the blood and then into the vascular endothelium, causing changes of the same nature as during epidemic typhus, although they are much less pronounced. In particular, there is no necrosis of the vascular wall, thrombosis and thrombohemorrhagic syndrome rarely occur. Endoperivasculitis and specific granulomas are most pronounced in the skin and to a much lesser extent in the brain. Allergic restructuring is more pronounced than in epidemic typhus. The transferred disease leaves a strong immunity, recurrent diseases are not observed.
Symptoms and course. Incubation period ranges from 3 to 7 days, rarely - up to 10 days. There are no prodromal phenomena (with the exception of the primary affect, which develops soon after a tick bite). As a rule, the disease begins acutely, with chills, body temperature rises, general weakness, severe headache, pain in muscles and joints appear, sleep and appetite are disturbed. Body temperature in the first 2 days of illness reaches a maximum (39-40°C) and then persists as a constant type of fever (rarely remitting). The duration of fever (without antibiotic treatment) most often ranges from 7 to 12 days, although in some patients it lasts up to 2-3 weeks.
When examining the patient, mild hyperemia and puffiness of the face are noted. Some patients experience hyperemia of the mucous membrane of the soft palate, uvula, and tonsils. The most typical manifestations are primary affect and exanthema. When bitten by uninfected ticks, the primary affect never develops; its presence indicates the onset of the infectious process. The primary affect is an area of ​​infiltrated moderately compacted skin, in the center of which necrosis or a small ulcer covered with a dark brown crust is visible. The primary affect rises above the skin level, the zone of hyperemia around the necrotic area or ulcer reaches up to 2-3 cm in diameter, but there are changes of only 2-3 mm in diameter and are quite difficult to detect. Not all patients note the very fact of a tick bite. Healing of the primary affect occurs after 10-20 days. In its place there may be pigmentation or peeling of the skin.
Characteristic The manifestation of the disease is exanthema, which is observed in almost all patients. It usually appears on the 3-5th day, rarely on the 2nd or 6th day of illness. First it appears on the limbs, then on the torso, face, neck, and buttocks. The rash is rarely observed on the feet and palms. The rash is abundant, polymorphic, consists of roseola, papules and spots (up to 10 mm in diameter). Hemorrhagic transformation of rash elements and the appearance of petechiae are rarely observed. Sometimes there is a “sprinkling” of new elements. The rash gradually disappears by the 12-14th day from the onset of the disease. There may be peeling of the skin at the site of the spots. In the presence of primary affect, it is usually possible to detect regional lymphadenitis. Lymph nodes are enlarged to 2-2.5 cm in diameter, painful on palpation, not fused to the skin and surrounding tissues, suppuration of the lymph nodes is not observed.
On the part of the cardiovascular system, bradycardia is noted, a decrease in blood pressure, arrhythmias and changes in the heart muscle according to ECG data are rare. Changes in the central nervous system are observed in many patients, but do not reach the same extent as occurs with epidemic typhus. Patients are bothered by severe headaches, insomnia, patients are inhibited, agitation is observed rarely and only in the initial period of the disease. Mildly expressed meningeal symptoms are very rarely detected (in 3-5% of patients); when examining cerebrospinal fluid, cytosis usually does not exceed 30-50 cells in 1 μl. There are no pronounced changes in the respiratory system. Enlargement of the liver is observed in half of the patients, the spleen increases less frequently (in 25% of patients), the increase is moderate.
Course of the disease benign. After the temperature drops to normal, the patients' condition quickly improves and recovery occurs quickly. Complications, as a rule, are not observed. Even before the use of antibiotics, the mortality rate did not exceed 0.5%.
Diagnosis and differential diagnosis. Epidemiological prerequisites (stay in endemic foci, seasonality, tick bites, etc.) and characteristic clinical symptoms in most cases make it possible to diagnose the disease. Primary affect, regional lymphadenitis, profuse polymorphic rash, moderate fever and benign course are of greatest diagnostic importance.
It is necessary to differentiate from tick-borne encephalitis, hemorrhagic fever with renal syndrome, typhoid and typhus, tsutsugamushi fever, syphilis. Sometimes in the first days of the illness (before the appearance of the rash), an erroneous diagnosis of influenza is made (acute onset, fever, headache, facial flushing), but the absence of inflammatory changes in the upper respiratory tract and the appearance of a rash make it possible to refuse the diagnosis of influenza or acute respiratory infections. Epidemic typhus and tsutsugamushi fever are much more severe with pronounced changes in the central nervous system, with hemorrhagic transformation of the elements of the rash, which is not typical for tick-borne typhus in North Asia. With syphilis, there is no fever (sometimes there may be a low-grade temperature), signs of general intoxication, a profuse, polymorphic rash (roseola, papules), which persists for a long time without much dynamics. Hemorrhagic fever with renal syndrome is characterized by severe kidney damage, abdominal pain, and a hemorrhagic rash. To confirm the diagnosis, specific serological tests are used: RSK and RIGA with diagnosticums from rickettsia. Complement-fixing antibodies appear from the 5-10th day of illness, usually in titers of 1:40-1:80 and subsequently increase. After the illness, they persist for up to 1-3 years (in titers 1:10-1:20). In recent years, the indirect immunofluorescence reaction has been considered the most informative.
Treatment. As with other rickettsioses, the most effective are tetracycline antibiotics. This can even be used for diagnostic purposes: if, when tetracyclines are prescribed after 24-48 hours, there is no improvement and normalization of body temperature, then the diagnosis of tick-borne typhus of North Asia can be excluded. For treatment, tetracycline is prescribed at a dose of 0.3-0.4 g 4 times a day for 4-5 days. If you are intolerant to antibiotics of the tetracycline group, you can use chloramphenicol, which is prescribed orally at 0.5-0.75 g 4 times a day for 4-5 days. Anticoagulants are not prescribed; the need for them arises only in rare cases of severe disease or with the development of hemorrhagic syndrome.
Forecast favorable. Even before the introduction of antibiotics, the mortality rate did not exceed 0.5%. The recovery is complete, no residual effects are observed.
Prevention and measures in the outbreak. A set of anti-tick measures is carried out. Persons working in natural areas must use protective clothing that protects a person from ticks crawling onto his body. Periodically, it is necessary to conduct self- and mutual examinations in order to remove flares that have crawled onto clothing or the body. When using regular clothing, it is recommended to tuck the shirt into trousers secured with a belt, fasten the collar tightly, tuck the trousers into boots, tie the sleeves with twine or tighten them with an elastic band. Persons exposed to tick bites and in whom primary affect is detected can be prescribed a course of tetracycline without waiting for the disease to develop. Specific prevention not developed.