Tularemia treatment with cardiovascular agents. Means for internal use. Tularemia in the USSR

Symptoms are primary local ulceration, regional enlargement of lymph nodes, general signs of intoxication, and sometimes atypical pneumonia. Diagnosis is primarily epidemiological and clinical and is confirmed by serological tests. Treatment is streptomycin, gentamicin, chloramphenicol, or doxycycline.

It is characterized by specific, regional lymphadenitis, fever, moderate intoxication, damage to various organs, a tendency to a wavy, protracted course.

Pathogenesis and pathology. The pathogen enters the body through the skin, mucous membranes of the eyes, respiratory tract, mouth, intestines. The pathogen penetrates into the lymph nodes, a bubo is formed, the death of the pathogen in the lymph nodes and blood, endotoxin is released. A generalization of the process outside the entrance gate may develop: the liver, spleen, lymph nodes increase, secondary buboes form, allergization of the body develops, HRT, granulomas and areas of necrosis in the liver, spleen, lymph nodes and kidneys, in the lungs, brain, exudate in the pleural cavity, as well as venous congestion and fatty degeneration in the heart, kidneys, dystrophic changes are formed.

Epidemiology of tularemia in humans

Sources of infection: more than 80 species of animals.

Ways of transmission: transmissible (mosquitoes, horseflies, ticks), food and water, contact, aspiration (dust inhalation). Transmissive and contact in summer, air-dust - autumn-winter-weight-on. Throughout the Russian Federation, rural residents, fishermen, livestock breeders, workers in vegetable stores, slaughterhouses, and housewives are more likely to get sick.

Causes of tularemia in humans

Polymorphic bacillus Fransiella tu-larensis.

There are 7 clinical syndromes associated with tularemia. The pathogenic organism, F. tularensis is a small, pleomorphic, non-motile, non-spore-forming aerobic bacillus that enters a living organism in the following ways:

• ingestion of contaminated food or water;
• bite of an infected arthropod (tick, deer fly, flea);
• airborne way;
• direct contact with infected tissue or material.

The microorganism can penetrate through seemingly whole skin, but can actually enter through microcracks.

There are 2 types of F. tularensis: type A and type B. Type A, the more virulent human serotype, is commonly found in rabbits and rodents in the US and Canada. Type B usually causes mild ulcerative glandular infection and occurs in aquatic animals in Europe and Asia.

Hunters, butchers, farmers and fur processors are commonly infected. During the winter months, most cases are the result of contact (especially during flaying) with infected wild rabbits. During the summer months, infection is usually the result of handling the skins of infected animals or birds, or the bites of infected ticks or other arthropods. Rare cases are the result of eating undercooked meat, contaminated water, or mowing in endemic areas. In the West, ticks, deer flies, horse flies and direct contact with infected animals are also sources of infection. Nothing is known about human-to-human transmission. Laboratory workers are at particular risk because infection is rapidly transmitted when handling contaminated materials. F. tularensis is considered a possible agent of bioterrorism.

In disseminated cases, characteristic focal necrotic lesions at various stages of development are scattered throughout the body. Their size is from 1 mm to 8 cm, they have a whitish-yellow color; appear externally as primary lesions on the fingers, eyes, or mouth and usually appear on the lymph nodes, spleen, liver, kidneys, and lungs. With pneumonia, necrotic foci appear in the lungs. Although there may be severe systemic toxicity, no specific toxins are found.

View	Frequency	Note
Ulcerous glandular	The most common	Primary lesions on the hands or fingers with regional lymphadenitis
typhoid	Common	Systemic disease without evidence of site of infection or localized infection
Oculoglandular	Uncommon	Unilateral inflammation of the lymph nodes, possibly caused by eye infection through contact with an infected hand or finger
glandular	rare	Regional lymphadenitis without primary lesion and neck adenopathy, suggesting oral bacterial entry
Pneumonic	Uncommon	Infiltrates with asymmetric intrathoracic lymphadenopathy with or without pleural effusion
Oropharyngeal	rare	Sore throat and cervical lymphadenopathy due to ingestion of contaminated water and food
Septicemic	rare	Systemic disease with hypotension, acute respiratory distress syndrome, disseminated intravascular coagulation, and multiple organ failure

Symptoms and signs of tularemia in humans

The onset is sudden, 1-10 (usually 2-4) days after infection, with headache, fever 39.5° to 40° C, and severe general weakness. Recurrent chills and profuse sweating are characteristic. Clinical manifestations depend to some extent on the type of infection.

Within 24-48 hours, an inflamed papule appears at the site of the lesion, with the exception of glandular or typhoid tularemia. The papule quickly becomes a pustule and turns into an ulcer with a clear ulcer crater with a scanty, thin, colorless exudate. Ulcers are usually solitary on the extremities, but multiple in the mouth or eyes. Usually only one eye is affected. Regional lymph nodes are enlarged, may suppurate and then drain. By day 5, a typhoid-like condition often develops, and the patient may develop atypical pneumonia, sometimes accompanied by delirium.

Pneumonic tularemia can begin after airborne or hematogenous infection with another type of tularemia; it develops in 10-15% of cases of ulcerative glandular tularemia and in approximately 50% of cases of typhoid tularemia. Although signs of lung tissue infiltration are often present, decreased breathing and intermittent wheezing may be the only physical manifestations of pneumonia in tularemia. A dry, nonproductive cough is associated with a burning sensation in the retrosternal region. A nonspecific rash similar to roseola may appear at any stage of the disease. Splenomegaly and perisplenitis may also be seen.

Mortality approaches zero with treatment and is approximately 6% in untreated cases of ulcerative glandular tularemia. Mortality is higher in type A infection and in typhoid, septicemic, and pneumonic tularemia; it reaches 33% in the absence of treatment. Death usually occurs with a generalized infection, pneumonia, meningitis, or peritonitis. Relapses can occur in case of improper treatment. As a result of the disease, immunity is developed.

The clinical form depends on the route of infection. With the air-dust path, a pulmonary, ocular-bubonic form develops. With laboratory infection with highly virulent strains, a generalized form develops with severe intoxication. Symptoms of intoxication of the initial period are common to all clinical forms: anorexia, insomnia, myalgia, sweating, nausea, vomiting, lymphadenitis (on the neck, armpits, groin) at the site of concentration and reproduction of the pathogen. On the 1st-3rd day of illness - hyperemia of the face, conjunctiva, roseolous-papular rash, enlargement of the liver and spleen, bradycardia, decrease in blood pressure.

Ulcerative bubonic form: a small spot is formed, sharply limited and turning into a papule, a vesicle with necrosis in the center, an ulcer with pus and inflammation around in a diameter of 10 mm or more. An increase in lymph nodes is a bubo, then the sore is covered with a dark crust, and a scar is slowly formed. The bubo is painless or slightly painful, mobile, dense, with a clear contour.

Oculo-bubonic form: edema of the eyelid is formed, pronounced conjunctivitis. Papules, sores with pus form on the mucous membranes of the eyes. Lymphadenitis (buboes) in the submandibular and parotid region.

Anginal-bubonic form: slight hyperemia of the oropharyngeal mucosa, an increase in one tonsil, an island or membranous plaque on it, there may be ulcers, necrosis, regional lymphadenitis (cervical, submandibular). The ulcers are deep and heal slowly. There may be damage to the mucous membrane of the palate, pharynx, mouth.

Abdominal shape: the tongue is lined, on palpation of the abdomen, soreness around the navel or to the right and downward from it. Inflammation of the mesenteric lymph nodes. Recover slowly.

Pulmonary form: pneumonia develops, it can be in the form of severe or easy flowing, like influenza, SARS, bronchitis.

Generalized septic form: may be typhoid. Recover slowly.

Diagnosis of tularemia in humans

• crops
• Serological analysis in the acute stage and in the recovery period

Diagnosis is based on evidence of contact with rabbits or wild rodents or infection from an arthropod vector, sudden onset, and a characteristic primary lesion.

Patients should have blood cultures and appropriate clinical material. Conventional cultures may be negative, the laboratory must be notified that tularemia is suspected so that appropriate media can be used (and proper precautions provided). Acute and convalescent antibody titers should be taken 2 weeks apart (a 4-fold increase or one titer >1:128 is diagnostic). Serum from patients with brucellosis may cross-react with F. tularensis antigens, but these are usually much lower titers. Some laboratories use fluorescent antibody staining.

Because this microorganism is highly contagious, specimens and media suspected of having tularemia should be handled with extreme care and, if possible, in a laboratory with high level (level 3) biosecurity equipment.

Diagnosis based on:

• passport data (place of residence, profession);
• medical history;
• epidemiological data (contact with animals, insect bites, ticks), hobbies (hunting, fishing), working with pathogens in the laboratory, being in the forest, in the countryside. Swallowing water from reservoirs while bathing, drinking water from random sources, drinking unboiled milk, working with hay, grain;
• complaints;
• clinical picture;
• laboratory research - serological, RA, RIGA, ELISA;
• biological sample;
• immunofluorescent study;
• immunological research - PCR;
• accelerated serological methods.

Differential diagnosis is carried out with typhus, tonsillitis, diphtheria, pneumonia, leptospirosis, Q-li-fever, brucellosis, meningoencephalitis, plague, anthrax, tuberculosis, malaria, sepsis, mononucleosis, relapsing fever, lymphadenitis vulgaris, Sodoku disease.

Treatment of tularemia in humans

• Streptomycin (plus chloramphenicol for meningitis).

Streptomycin is the drug of choice. Chloramphenicol is added if there is evidence of meningitis.

Alternatives to streptomycin are gentamicin, doxycycline, chloramphenicol, and ciprofloxacin. However, relapses are sometimes observed with these drugs, and they may not prevent the nodule from suppurating.

Permanent moist hypertonic dressings are useful for primary skin lesions and may reduce the severity of lymph node inflammation and lymphadenitis. Surgical drainage of large abscesses is rarely necessary unless therapy is delayed. In severe cases, 2% gomatoprim 1-2 drops every 4 hours may relieve symptoms. Severe headache is usually relieved by oral opioids (eg, oxycodone or hydrocodone with acetaminophen).

Prevention of tularemia in humans

When entering endemic areas, people should wear protective clothing against ticks and repellents. Inspection for ticks should be done after leaving tick-infested areas. Ticks should be removed immediately.

There is currently no vaccine. Antibiotic prophylaxis with doxycycline or oral ciprofloxacin for 14 days is recommended after a possible infection (eg, laboratory accident).

Tularemia (plague-like disease, rabbit fever, small plague, deer-fly fever, mouse disease, epidemic lymphadenitis) is an acute zooantrapanous natural focal bacterial infection with multiple transmission mechanisms, characterized by a fever-intoxication syndrome, inflammatory changes in the entrance gates of infection and regional lymphadenitis.

The disease was first established in 1911 in California, when McCoy and Chepii discovered a plague-like disease in ground squirrels, isolated the pathogen and named it Bacterium tularense (after the epizootic site in the Tulare Lake area). Later, they discovered the predisposition of this disease in humans, and some time later they learned about the scale of prevalence: throughout North and Central America, on the Eurasian continent. In general, it is believed that the disease exists where rodents actively breed.

Francisella tularensis is a gram-negative bacillus (that is, it turns pink) and this color indicates the presence of a capsule, therefore, some phagocytic protection when it enters the macroorganism. It has no spores or flagella. There are also other structural features of the pathogen that create features of the symptoms:

Neurominidase promotes adhesion (attachment) to the affected tissues;
endotoxin causes fever-intoxication syndrome and allergenic properties of the cell wall;
the ability to multiply in phagocytes and suppress their killer effect;
The presence of receptors for Fc fragments of immunoglobulin class G (IgG), therefore, the activity of complement systems and macrophages is impaired.

The last two factors lead to an allergic restructuring of the immune system.

The pathogen is relatively stable in the external environment (despite the absence of sporulation), especially at low temperatures and high humidity: it survives at "-300 ° C", in ice - up to 10 months, in frozen meat up to 3 months, in water - more than a month (and at 10°C - 9 months), in excretions from sick rodents - more than 4 months, in soil - 2.5 months, in milk - 8 days, at a temperature of 20-30°C - up to 3 weeks.

The pathogen is sensitive to the following factors:

High temperature - at 60 ° C dies within 10 minutes;
direct UVI - dies in 30 minutes;
Ionizing radiation and disinfectants (3% lysol, 50% alcohol, formalin, chloramine, bleach, sublimate) are detrimental - inactivation of the pathogen occurs after 10 minutes.

The susceptibility of people to tularemia is high and reaches 100%, that is, everyone who has contact with the pathogen will get sick, without gender and age restrictions. There is a summer-autumn seasonality. Natural focal prevalence - natural foci of tularemia exist on all continents of the northern hemisphere, in the countries of Western and Eastern Europe, Asia and North America. On the territory of the Russian Federation, the disease is recorded everywhere, but mainly in the Northern, Central and West Siberian regions of Russia.

Causes of tularemia infection

The source is about 150 species of vertebrates (105 mammals, 25 species of birds, some aquatic organisms), but a detachment of rodents (voles, water rats, house mice, hares) occupies a place of honor, in the third place - livestock (sheep, pigs and cattle cattle).

The carrier is blood-sucking insects (ixodid and gamasid mites, mosquitoes, horseflies). Mechanisms of infection transmission: contact (during direct contact with infected animals or their biological materials), contact-household (when household items are contaminated with the waste of sick animals), alimentary (when eating contaminated food), transmissible (when bitten by infected bloodsuckers), aerogenic (when inhalation of contaminated dust).

The pathogen enters the human body through microtraumas of the skin, intact mucous membranes of the tonsils / oropharynx / gastrointestinal tract / respiratory tract / eyes and possibly the genital organs. Moreover, for infection, only the minimum infectious dose is needed, and, in this disease, this dose is one microbial cell (while in other infectious diseases - 10 "⁵ or more)!

Symptoms of tularemia

The incubation period (the time from the beginning of the introduction of the pathogen to the onset of symptoms) is 2-8 days, but sometimes it can be delayed up to 3 weeks. During this period, the pathogen attaches and multiplies at the entrance gate, and as soon as the amount of the pathogen reaches a certain concentration, a period of clinical manifestations occurs.

The period of clinical manifestations is characterized by both local and general symptoms. Local changes - an inflammatory-necrotic reaction at the site of the pathogen, with the formation of a primary affect (skin ulcer, passing through the stages of papules, vesicles and pustules, if the primary contact occurred on the tonsils - necrotic tonsillitis, in the lungs - focal necrotic pneumonia, on the conjunctiva - conjunctivitis) .

But local reactions proceed and develop in parallel with the general ones, namely, regardless of the form of the disease (anginal, abdominal or pulmonary), an acute onset of the disease is noted (similar to a prodromal period, lasting 2-3 days) - with fever-intoxication syndrome (temperature rises to 38-40°C and above, headache, dizziness, general weakness, excessive sweating, loss of appetite, bradycardia, hypotension).

General intoxication symptoms are explained by the fact that some of the pathogens remain at the gates of infection and form the primary focus, and some spread along the lymphogenous and hematogenous pathways. After attaching, the pathogen penetrates into the lymphatic vessels and reaches the regional lymph nodes, where it multiplies unhindered and thus edema forms in the lymphoid tissue and a "bubo" is formed (as in the case of plague), after which the pathogen penetrates into the blood and causes bacteremia, it is carried by the blood stream into organs and tissues, as a result of which granulomas and necrotic ulcers are formed in them, a variety of symptoms are formed.

But the variability of clinical forms depends mainly not on the affected organs, but on the location of the entrance gate, according to which the following clinical forms of tularemia are distinguished:

Ulcerous glandular (bubonic),
oculo-glandular (conjunctivitis);
anginal-glandular;
abdominal;
pulmonary.

After the onset of bacteremia and infection of the organs, a peak period begins, characterized not only by a fever-intoxication syndrome (the duration of a high temperature reaches a month!), but also by various other symptoms with the same frequency of occurrence:

The appearance of patients is very characteristic: a puffy and hyperemic face, possibly with a bluish tint around the eyes / lips / earlobes, around the chin - a pale triangle, injection of scleral vessels, pinpoint hemorrhages on the oropharyngeal mucosa, erythematous / or papular / or petechial hemorrhages leaving behind peeling and pigmentation

Lymphadenitis of various localization. When a bubo occurs (a very large lymph node - from a walnut to 10 cm in diameter) - they talk about the BUBONY FORM, which occurs during transmixing infection mechanisms, localization is more often - femoral, inguinal, ulnar, axillary. And around this lymph node a conglomerate with signs is formed periadenitis. A bubo appears on the 2-3rd day from the onset of clinical manifestations and reaches its dawn by the 5-7th day, with a gradual increase in local changes: at first, the skin over the lymph node is not changed, but redness appears over time + the cohesion of this lymph node with the skin and surrounding tissues increases + Pain increases. The outcome of this bubo can be different - from traceless resorption to suppuration with fluctuation and subsequent scarring (in this case, the bubo is filled with plum pus, which resolves and heals for several months, leaving a scar behind).

Bubo in tularemia

In the ULCER-BUBON FORM - lymphadenitis is also observed, but already with skin changes in the gates of infection that come to the fore - a primary affect is formed at the site of introduction, which goes through stages from a spot - papules - pustules - a painless small ulcer (5-7 mm) with undermined edges and scanty serous-purulent discharge, and this ulcer heals within 2-3 weeks, leaving a scar behind. This form occurs both with transmissive and with contact / contact-household transmission mechanisms. The usual localization is open parts of the body (neck, forearm, lower leg).

With ANGINOUS-BUBONIC FORM, lymphadenitis takes second place, and angina comes to the fore with some features: hyperemia of the tonsils with a bluish tint and swelling, grayish-white island or membranous plaque - it is difficult to remove and therefore it can be confused with diphtheria films, but in unlike the latter, films with tularemia do not extend beyond the tonsils. After a few days, slowly healing ulcers form under these plaques (in rare cases, they can even appear to the film). This form occurs during alimentary infection, and the abdominal form may later join this form.

ABDOMINAL FORM (gastrointestinal) - the rarest, but the most severe form. The clinic is very variable: cramping or aching pain, diffuse or localized, the tongue is coated with a grayish-white coating and is dry, dyspeptic symptoms (both constipation and stool liquefaction are possible)

The EYEBUBONIC FORM occurs when the pathogen enters through the conjunctiva through contaminated hands, with high air contamination - that is, by air-dust. With this form, conjunctivitis occurs (usually unilateral), with severe lacrimation and eyelid edema, pronounced swelling of the transitional fold, mucopurulent discharge, the presence of yellowish-white nodules on the mucous membrane of the lower eyelid. At the same time, regional lymph nodes increase - behind the ear, submandibular, anterior cervical.

PULMONARY FORM (THORACAL) occurs when infected by airborne droplets and can proceed either in bronchitis or in pneumonic form. In the bronchitis form - dry cough, pain behind the sternum, hard breathing and dry wheezing. This form is milder than pneumonia and clinical recovery occurs after 2 weeks on average.

Diagnosis is based on epidemic, clinical and laboratory data. An epidemiological study establishes a connection and time frame between the clinic and recent departures. Due to the vastness and blurring of symptoms, clinical data are uninformative.

Laboratory data are presented in a wide range:

- KLA: normotsitrz or leukocytosis (LC), neurocytosis (Nf), ESR. During the peak period - ↓Lc, Lf and M. With suppuration of buboes - neutrophilic leukocytosis.

Serological methods: RA (agglutination reaction) and RPHA (hemagglutination reaction) - determination of titers of antibodies and antigens 1: 100 and, the earliest method - RPHA, and RA allows you to detect an increase in antibody titer from 10-15 days, a second study is carried out after a week and , if the titer has not changed or they are not detected at all, the study is repeated after another week and, an increase in antibody titer by 2-4 times makes the diagnosis of tularemia eligible. ELISA (enzyme-linked immunosorbent assay) is 20 times more sensitive than all other serological methods, but it is advisable to use it from day 6 and indicates this method for the detection of specific antibodies - IgG and M, which determine the stage of the disease: in the presence of IgM they speak of an acute process or about the peak stage, and the presence of IgG indicates a later date from the moment of infection and indicates a good immune response.

The allergological method is the use of an allergic skin test, which is distinguished by strict specificity and is carried out from the 3rd day of the disease, therefore it is referred to as an early diagnostic method. It is carried out as a Mantoux test, but instead of tuberculin, tularin is injected into the middle part of the forearm and the result is evaluated at the end of the first day, on the second and on the third, measuring the diameter of the infiltrate: if the diameter of the infiltrate is more than 0.5 cm, the test is positive, if the hyperemia disappears at the end of the first day - is negative. If there are contraindications to performing a skin test, an allergological method is also carried out, but in vitro (that is, in a test tube and look at the leukocytolysis reaction).

The bacteriological method is aimed at detecting the pathogen in biological substrates, but it can only be carried out in specially equipped laboratories, because the pathogen is highly contagious (contagious), therefore such an analysis is rarely prescribed to patients.

PCR (polymerase chain reaction) - a genetic method aimed at detecting the DNA of the pathogen, is informative already in the febrile period, therefore it, like the allergological method, is classified as an early diagnostic method.

Treatment of tularemia

Treatment begins with compliance with the ward regime, in which the windows are covered with a mesh to prevent the transmission mechanism of transmission + strict adherence and control of sanitary and hygienic rules (current disinfection using a 5% phenol solution, sublimate solution and other disinfectants).

Etiotropic therapy is aimed at the destruction of the pathogen by the use of antibiotics of the aminoglycoside and tetracycline series. If there is an allergy to aminoglycosides, then third-generation cephalosporins, rifampicin, chloramphenicol, fluoroquinolones used in age doses are used as an alternative. Streptomycin - in the national guidelines for infectious diseases they write about applicability for tularemia, but they try to resort to it rarely and only in a hospital, because it blocks neuromuscular conduction with subsequent respiratory arrest. Gentamicin - 3-5 mg / kg / day for 1-2 doses, Amikacin - 10-15 mg / kg / day for 2-3 doses. Tetracyclines are prescribed for bubonic and ulcerative bubonic form; Do not prescribe them to children under 8 years of age, pregnant women, patients with decompensation from the kidneys and liver. The course of antibiotics is 10-14 days.

Local therapy - for skin ulcers and buboes, consists in the use of antiseptic dressings, quartz, blue light and laser irradiation. When suppuration of the bubo is a surgical intervention, which consists in opening the bubo with a wide incision to empty it of pus.

Patonenetic therapy consists in the appointment of detoxification, antihistamine, anti-inflammatory drugs, vitamin complexes and cardiac glycosides - according to indications. You should also remember about the prevention of dysbacteriosis when using antibiotics - pre / probiotics are prescribed and, not only orally, but also rectally, because when passing through the gastrointestinal tract, bifidum and lactobacilli die in the acidic environment of the stomach.

Complications of tularemia

On the part of the immune system - allergic reactions, IDS (immunodeficiency states); But since there are no specific target organs, there is no specific clinic, therefore there are no specific complications, but there are the most common (possibly due to infection gates): ITSH (infectious toxic shock), meningitis, pericarditis, myocardial dystrophy, polyarthritis, peritonitis, corneal perforation, bronchiectasis, abscesses and gangrene of the lungs.

Prevention of tularemia

Prevention is divided into specific and non-specific. Specific - the use of a live dry tularemia vaccine, for children over 7 years old, staying in tularemia endemic territories, the state of immunity is assessed by serological tests on days 5 (7) and 12 (15), for 5 years, and 1 time in 2 years, with negative indicators carry out revaccination.

Non-specific prevention consists in monitoring natural foci, timely detection of outbreaks of the disease among wild animals, carrying out deratization and disinfestation.

With a water outbreak - it is forbidden to swim in this water and drink unboiled water. Apply specialized clothing when in contact with sick animals or when in their habitats.

The doctor's consultation:

Question: Do I need to open the vesicle at the site of the bite?
Answer: no.

Question: Is immunity preserved after the disease?
yes, it is persistent, durable, lifelong; It has a cellular nature (due to T-lymphocytes, macrophages and antibodies), phagocytosis in immunized is complete, in contrast to the infected.

Therapist Shabanova I.E

The media do not mention this disease and doctors do not talk about it, since tularemia is rare in the northern latitudes. Although there are no mass epidemics in Russia, the pathology does not become easily tolerated and less dangerous. According to the definition, tularemia is an acute infection that occurs with damage to the internal organs and lymph nodes. Along with anthrax, cholera and plague, it is ranked among the most dangerous infectious diseases for humans.

What is tularemia

The first information about tularemia (tularemia) reached the civilized world at the beginning of the 20th century, when American scientists discovered ground squirrels near Lake Tulare with signs of a plague-like disease. In 1911, the pathogen was isolated and named Bacterium tularensis. Some time later, this bacterium was found in many European countries - Norway, France, Austria, Germany, Sweden. Cases of the disease have been registered in the countries of America, Asia, Turkey and Russia.

Tularemia (rabbit fever, epidemic lymphadenitis, plague-like or mouse disease, deer fly fever, small plague) is an acute zooantrapanosis focal infection of a bacterial nature. Pathology is caused by small bacteria - tularemia bacilli that live in the environment and the body of animals. The main carriers of Bacterium tularensis are blood-sucking insects.

Pathogen

There are several species of Francisella tularensis. There are two subspecies A and B, which differ in the degree of pathogenicity. The first is characterized by an extremely high ability to cause an infectious process. Subspecies B has less pathogenicity, provoking mild forms of tularemia. According to the continents, the Central Asian, American, European-Asian and Holarctic species Francisella tularensis are distinguished.

The causative agent of tularemia is poorly resistant to high temperatures (boiling, ultraviolet radiation). Lysol, chloramine, bleach and chemicals kill bacteria in 3 minutes. At the same time, the pathogen lives in straw and grain for up to six months, and lives in animal corpses for up to 8 months. Francisella tularensis persists for a long time in meat and milk.

carriers

The pathogen enters the body of an animal after a bite from a horsefly, mosquito, tick or other arthropod. Small rodents are more likely to become infected - field mice, muskrats, chipmunks, but large animals can also be carriers of the infection. A person becomes infected by contact with infected meat, skinning carcasses, collecting rodents, and so on. The source of infection is contaminated water and air. The pathogen cannot pass from a sick person to a healthy one.

Tularemia carriers are more than 60 species of different animals, upon contact with which a person can become infected. Tularemia affects children, the elderly and young people equally. The spread of the disease does not depend on sex, race and age. Groups of persons included in the risk category:

• hunters;
• housewives who live in areas where infection is often recorded;
• anglers catching infected fish;
• slaughterhouse workers,

• contact (touching an infected animal);
• alimentary (consumption of contaminated water or food);
• air-dust (by inhalation of infected air particles);
• transmissible (after the bite of an infected blood-sucking insect).

After an infection enters the body, the lymph nodes are the first to be affected. Further spread of francisella tularensis occurs through the lymphatic system. The human body tries to cope with the pathogen, but during the death of pathogenic bacteria, endotoxin is released, which worsens the situation. If the lymphatic system fails, the infection enters the bloodstream, after which it spreads to the internal organs.

signs

Tularemia can have a short incubation period - no more than a few hours, or a long one - about three weeks. In most cases, it lasts from 3 to 7 days. The prolonged or abrupt onset of the disease depends on the type and amount of the pathogen that has entered the human body. An important place in the intensity of the disease depends on the immunity of the sick person. The first symptoms of tularemia are similar to numerous signs of acute infections:

• chills;
• body temperature rises to 40 °;
• severe headache;
• aching muscles and joints;
• dizziness, weakness.

During the examination of the patient, the doctor notes swelling and redness of the face, injection of the sclera or an increase in the vascular network of the eyes, plaque on the tongue, hemorrhages on the oral mucosa. The patient has enlarged lymph nodes, and the localization of inflammation depends on the place of introduction of the pathogen. In the later stages of infection, other signs are observed:

• blood pressure decreases;
• the pulse becomes rare;
• on the 3rd-5th day of the disease, a dry cough appears;
• During the examination, most patients have an enlarged spleen and liver.

Classification

According to the course of the disease, mild, moderate and severe are distinguished, and according to the duration - acute, protracted, chronic, recurrent. There are three clinical forms of tularemia, which are classified according to the site of development of the infectious process:

• damage to internal organs: abdominal, hepatic, bronchopneumonic, pulmonary and others;
• weakened immunity: generalized;
• damage to the skin, lymph nodes, mucous membranes: ulcerative-bubonic, bubonic, oculobubonic, angio-bubonic.

Diagnostics

The correct diagnosis depends on the timely collected anamnesis. The doctor collects any information about the patient: recent contacts, the presence of hunting or fishing, insect bites. Non-specific laboratory methods (urinalysis, blood tests) show signs of intoxication and inflammation. In the first days after infection, neutrophilic leukocytosis is observed in the blood, and then the number of leukocytes decreases, the concentration of monocytes and lymphocytes increases.

Specific serological diagnostics are RIHA and RA (reactions of indirect hemagglutination and direct agglutination). If the disease progresses, the titer of specific antibodies increases. On the 7th-10th day of illness, it is possible to determine the infection using ELISA (immunofluorescent analysis). This is the most sensitive test for tularemia. In the early days of fever, PCR is sometimes used. Rapid diagnosis of tularemia is carried out using a skin-allergic test - it gives the result already on the 3rd day of the disease.

Bacteriological culture is rarely performed, since the isolation of bacteria and other biomaterials from the blood is difficult. On the 7th day of the disease, it is possible to isolate the pathogen by bakposev by examining the punctate of buboes or the discharge of ulcers, but the laboratory tools needed for this analysis of the culture are very rare. In the pulmonary form of infection, a CT scan of the lungs or X-ray is performed.

Complications

In most cases, the prognosis of tularemia infection is favorable. Lethal outcomes were registered in only 0.5% of cases. More often complications are given by the generalized form of the disease. Possible consequences of tularemia:

• inflammation of the membranes of the brain (meningitis, meningoencephalitis);
• chronic joint damage (polyarthritis);
• secondary pneumonia;
• progressive cardiac pathologies (myocardial dystrophy);
• infectious psychosis;
• chronic course of the infectious process with frequent relapses.

Treatment of tularemia

In order to avoid the development of severe complications and infection of people around, tularemia is treated in an infectious diseases hospital. The patient is discharged only after complete recovery. An important step in the treatment of this infection is detoxification of the body. To do this, prescribe colloidal solutions (Reamberin, Polivedon) in combination with vitamins of group B. Additionally, the tactics of forced diuresis are used - diuretic drugs are administered to artificially stimulate urination.

Specific therapy begins with the appointment of a course of antibacterial agents. Tetracycline antibiotics are mainly used (Doxycycline, Gentamicin, Tetracycline). If the prescribed drugs are ineffective, second-line antibacterial agents are prescribed - these are third-generation cephalosporins (Rifampicin, Chloramphenicol). With severe intoxication, intravenous infusion of glucose and electrolyte solutions is performed.

Detoxification therapy includes taking non-steroidal anti-inflammatory drugs (Diclofenac, Ibuprofen), antihistamines (Diazolin, Suprastin), antipyretics (Salicylic acid, Aspirin), painkillers (Analgin, Ketanov), vitamin and mineral complexes (Complivit, Alfavit). If necessary, cardiovascular therapy is prescribed. Ulcers formed on the skin are covered with sterile dressings. If festering buboes are present, then they are surgically opened and drained.

A vaccine is used to prevent infection with the tularemia bacillus. Its purpose depends on the epidemiological characteristics of different foci of infection. Routine vaccination is carried out in areas with a high risk of infection. The vaccine is prescribed for all age groups, starting from 7 years. People who need vaccination are determined by the sanitary and epidemiological supervision. Among them:

Personal protective measures are needed when hunting wild animals (skinning and butchering) or when collecting dressed rodents. Hands must be protected with gloves and thoroughly disinfected. To stop the alimentary route of infection, it is necessary to avoid the ingestion of liquids from unknown reservoirs and other unreliable sources. It is advisable to limit visits to the infected forest and drink only boiled water.

Video

The causative agent of tularemia, Francisella, is a very small polymorphic bacterium. Enter the department Cracilicutes, section 4 (gram-negative aerobic rods and cocci). Genus Francisella represented by two types, one of them - Francisella tularensis - pathogenic. This species causes a natural focal infectious animal disease - tularemia - characterized by fever, paralysis in young animals, swollen lymph nodes, and abortions.

The tularemia bacterium was isolated in 1912 by McCoy and Chapin while studying a plague-like disease in ground squirrels in Tulare County (California). Genus Francisella named after Francis, who first studied the biology of this microbe. Inside the View F. tularensis three geographical races are distinguished: Holarctic, Central Asian and Nearctic, differing in some biological features.

Morphology. IN On stained smears, the causative agent of tularemia has a coccoid or rod-shaped shape 0.3–0.7 μm in length and 0.2–0.4 μm in width; there are smaller cells (0.15 μm or less) that can pass through bacterial filters. Coccoid forms are more often found in cultures, rod-shaped - in animals. The bacterium is characterized by polymorphism, which is revealed during growth on nutrient media: preparations from cultures, along with typical bacteria, can contain spherical and filamentous forms.

The microbe is immobile, does not form spores, has a small capsule; in cultures, it produces mucus, which is easily detected in the manufacture of smears.

The causative agent stains with all aniline dyes, but noticeably paler than other bacteria, gram-negative. In smears-imprints from the organs of dead animals, it is well painted according to Romanovsky-Giemsa, acquiring a lilac color. In tissues, bacteria do not stain bipolarly, which is how they differ from Pasteurella.

Cultivation. The bacterium does not grow on universal nutrient media. For its cultivation, McCoy's rolled yolk medium (60% egg yolk and 40% saline) is used. Francis medium (2.5% meat-peptone agar, 0.1% cystine, 1% glucose and 5-10% defibrinated rabbit blood), Drozhevkina's semi-liquid yolk medium (10% chicken yolk and 90% sterile saline), blood fish - Yeast agar with glucose and cystine, etc.

The tularemia bacterium is a strict aerobe, the optimum temperature is 36-37 0 C, the pH of the medium is 7.2-7.0. On a coagulated yolk medium, with abundant growth, microbes grow in the form of a shiny thin coating with a sinuous (“shagreen”) surface; with poor growth, small, shiny, raised colonies or groups of colonies grow. On the Francis medium, the culture looks like small (1-2 mm) round, convex, smooth, shiny, with smooth edges, whitish colonies with a bluish tint; growth is noted in 2-3 days. Colonies of pathogenic strains are S-shaped. In liquid nutrient media, the tularemia microbe grows much worse (only on the surface of the medium). Bacteria also multiply well in the yolk sac of a developing chicken embryo.

biochemical properties. The tularemia bacterium does not have a pronounced biochemical activity. The ability to ferment carbohydrates and alcohols is limited and can only be reliably detected on special dense media with a reduced protein content and a certain pH. Hiss media are unsuitable for this purpose. The microbe ferments with the formation of acid without gas glucose, maltose, in some cases - levulose and mannose; does not ferment lactose, sucrose, rhamnose, mannitol; forms hydrogen sulfide and reduces thionine, methylene blue, malachite green.

Antigenic structure. Pathogenic variants of the causative agent of tularemia (S-form) have two antigenic complexes localized on the cell surface. The first of them - Vi-antigen - contains lipids and proteins, determines the virulence and immunogenicity of the microbe; the second - O-antigen - is located in the cell wall and capsule-like layer of the bacterium, a thermostable glycoprotein. Both of these complexes have allergenic and antigenic properties, induce the formation of agglutinating, precipitating and complement-fixing antibodies, as well as delayed-type hypersensitivity. The function of the allergen in this bacterium is performed by a polysaccharide-polypeptide complex. The Vi antigen of pathogenic variants of the causative agent of tularemia is similar to that of Brucella.

Sustainability. IN in water or moist soil at 4 0 C it persists without a decrease in virulence for more than 4 months, in water at 20-25 0 C - 10-15 days, in grain and straw at temperatures below 0 0 C - up to 6 months, at 8-12 0 C - 56 days, at 20-30 0 C - no more than 20 days. In frozen meat, the pathogen is viable for up to 93 days, in milk and cream at 8-10 0 C - at least 3 weeks, in frozen milk - up to 104 days. In frozen corpses of animals that died from tularemia - more than 3 months, in their skins at 8-12 0 С - more than a month, at 32-33 0 С - 1 week. The microbe is resistant to drying.

It is especially sensitive to ethyl alcohol (it dies in 0.5-1 minutes). Sensitive to disinfectants - lysol, phenol, creolin, but most to bleach. Unresistant to many antibiotics - streptomycin, chloramphenicol, tetracycline, neomycin, kanamycin; resistant to penicillin.

Pathogenicity. The bacterium is pathogenic for hares, voles, house mice, ground squirrels, rats. Farm animals are relatively resistant to tularemia, they become ill sporadically, the disease often proceeds in a latent form. Lambs and piglets are the most susceptible, horses and donkeys get sick. In cattle, the disease is accompanied by swollen lymph nodes and mastitis. Buffaloes, camels, reindeer are sensitive. Adult sheep are resistant to the disease, goats are even more resistant. Susceptible rabbits, whose disease proceeds without characteristic signs and may resemble pseudotuberculosis and chronic pasteurellosis. Of the birds, chickens are susceptible, especially chickens. Guinea pigs and white mice are susceptible to infection.

A person also suffers from tularemia, but the disease proceeds relatively benignly and the patient does not pose a danger to others.

The true exotoxin in this microbe has not been isolated, but it synthesizes pathogenic enzymes: asparaginase, hyaluronidase, glutacinase, deaminase, transamidase, ronidase, fibrinolysins. Uronidase is found only in virulent strains. It is believed that the pathogenic effect of the tularemia microbe is mainly due to endotoxin.

Pathogenesis. Infection occurs by alimentary, airborne and transmissible routes. Bacteria can enter the body through intact skin, conjunctiva, respiratory tract. The causative agent, multiplying at the site of introduction, first enters the lymph nodes, then penetrates into the bloodstream and causes septicemia. The symptom complex is determined by the species and age resistance of animals, as well as the ability of the pathogen to multiply in organs rich in reticuloendothelial elements.

epidemiological data. The disease is registered in America, Europe, Asia and Africa, as well as in Russia. Most often, tularemia occurs during the years of mass reproduction of rodents. Rodents (field, house mice, gray and water rats, muskrats, etc.), hares, rabbits, etc. are susceptible to tularemia, they create a reservoir of the pathogen in nature. Agricultural animals are also sick, especially sheep, and lambs are most seriously ill. Of laboratory animals, white mice and rats, guinea pigs and rabbits are susceptible. Dogs and cats are insensitive to the pathogen. A very sensitive person.

The disease in farm animals is recorded sporadically, and in rodents, especially muskrats, it manifests itself as an epizootic. Outbreaks of tularemia are recorded seasonally (usually in spring and autumn) during the period of mass reproduction and intensive migration of rodents, as well as during the period of activity of blood-sucking insects. Natural foci of tularemia, which remain active for up to 50 years or more, are confined to the habitats of rodents. Outbreaks of tularemia in sheep are preceded by epizootics of this disease in hares.

Pre-mortem diagnostics. Clinical manifestation is observed only in sheep. In other animals it proceeds latently. In sheep, the temperature rises to 41.6 0 C, depression, unsteady gait, and later dragging of the buttocks, paralysis, diarrhea, anemia of the mucous membranes, coma.

Post mortem diagnostics. The phenomena of bacteremia with damage to the vessels of the lungs, spleen, heart, lymph nodes. The lymph nodes are markedly enlarged, with necrotic nodules or abscesses.

Laboratory diagnostics. When taking, delivering to the laboratory and examining the material for tularemia, the precautions provided for by the rules for working with especially dangerous infections are observed. The material for the study is the liver, kidney, spleen, enlarged lymph nodes taken from the corpses of large animals; corpses of rodents are sent entirely.

The material examination scheme includes bacterioscopy, isolation of pure cultures, and a biological sample.

Smears-prints from animal organs are stained according to Romanovsky-Giemsa; take into account large accumulations of lilac coccobacteria. Bacterioscopy should be considered as an indicative method.

To indicate bacteria, a direct immunofluorescence reaction is used, but this method is a signal method, and positive results must be confirmed by isolation of the pathogen culture. For this purpose, sowing of pathological material is carried out on special nutrient media (folded yolk medium of McCoy, Drozhevkina and Emelyanova media). At the same time, control crops are made on MPA and in BCH, which are incubated under aerobic and anaerobic conditions at a temperature of 37 0 C. With abundant inoculation, the growth of tularemia bacteria on a coagulated yolk medium appears in the form of a continuous plaque already after 18-24 hours and reaches a maximum after 2-3 days ; with poor sowing, individual colonies are noticeable on the 3rd-5th day and later. Therefore, inoculated media are recommended to be incubated for 10-14 days. On Drozhevkina's medium, the microbe grows diffusely and the presence of microbes is controlled by microscopic examination of smears. A freshly isolated culture is identified by morphological (non-motile coccobacteria), tinctorial (gram-negative bacteria) properties, growth pattern on folded yolk medium, absence of growth on universal nutrient media, and also by the results of test-tube RA with specific agglutinating serum.

biological test. The most sensitive and reliable method for the detection of tularemia bacteria in any material. They infect white mice, rarely guinea pigs. Suspension of pieces of organs and lymph nodes is administered at a dose of 0.5 ml subcutaneously or intraperitoneally or rubbed into a freshly trimmed area of ​​the skin. White mice die after 3-4 days, sometimes after 8-12 days, guinea pigs - on days 4-6, with a weak infection of the material - within 8-20 days.

Serological diagnosis. Carried out using reactions of agglutination, precipitation, indirect hemagglutination and neutralization of antibodies.

RA is a fairly accurate test for tularemia. The antigen is a tularemia diagnosticum prepared from microbial cells killed with formalin. RA is put in two ways: test-tube and blood-drop. Diagnostic titers for tularemia should be considered: for sheep - 1:25, for cattle and pigs - 1:100.

The reaction of indirect hemagglutination (RIHA) is performed with erythrocytes sensitized with a tularemia antigen or with an antibody erythrocyte diagnosticum. In the first case, it is used to study the sera of agricultural and wild animals for the presence of specific antibodies, in the second case, to determine the antigen in animal corpses. The precipitation reaction has a relatively low sensitivity, and it is used mainly in the study of rodent corpses.

allergic method. Delayed-type hypersensitivity in animals with tularemia develops early (until the fifth day of illness) and persists for a long time, so the allergic method can be used for early and retrospective diagnosis. The allergen is tularin; the drug is administered intradermally, the reaction is taken into account twice - after 24 and 48 hours.

specific prophylaxis. In sick animals, a stable and long-term immunity is created, which is based on tissue and humoral mechanisms. Agglutinins are found in the sera of recovered animals, and cellular defense reactions are formed quite early.

For prophylactic immunization of a person, a dry live vaccine against tularemia, proposed in 1946 by N. A. Gaisky and B. Ya. Elbert, is used.

No vaccine has been developed for farm animals.

Veterinary and sanitary assessment and activities. Sick animals are not allowed to be slaughtered. If tularemia is detected after slaughter, all slaughter products with the skin are destroyed. Carcasses and organs suspected of being contaminated with tularemia pathogens are sent for disposal.

The veterinary service of the enterprise is obliged to report all cases of detection before or after slaughter of sick animals with tularemia (in the prescribed manner) to the veterinary department of the regional (territorial) department of agriculture, the Ministry of Agriculture of the Russian Federation or the main department of veterinary medicine of the ministry and local health authorities at the location of this enterprise .

For disinfection of slaughter sites, a 2% solution of caustic soda or potassium (70 0 C), a 3% solution of xylonaphite-5, and a 2% solution of formaldehyde are used.

An acute infectious natural focal disease, which is characterized by fever, damage to the lymph nodes and skin, is tularemia. What it is?

Literally, the name comes from Tulare, a region in California where it was first isolated.

History and etiology

The causative agent is Francisella tularensis. It was first isolated in 1911 by employees of the anti-plague station G. Mc-Coy and Ch. Chapin from sick gophers in California. Later, in 1921, the disease was identified in humans. E. Francis called it tularemia.

Tularemia in the USSR

In the Soviet Union, tularemia was first diagnosed in humans in 1926 when S. V. Suvorov, A. A. Volferts, and M. M. Voronkova identified the pathogen from patients in a focus in the Volga delta. In the USSR, natural tularemia foci have been recorded everywhere, including in Chukotka, Kamchatka, Sakhalin and Primorsky Krai. The northernmost focus was found on the Pyasina River (Taimyr Peninsula), and the southernmost - in Azerbaijan. Only Kyrgyzstan is free from tularemia.

Zones unfavorable for tularemia are located in the northwest direction, in the central region, in the European southern and southeastern regions of the Soviet Union, as well as in the forest-steppe of Western Siberia, in Altai, Alatau and Tien Shan. In other regions, the infection is fixed mainly in river valleys, and in the Transcaucasus - in the foothills and mountainous regions.

In the Second World War and until 1949, due to an increase in the number of rodents (due to the remaining unharvested fields due to military operations), the incidence of tularemia increased significantly.

In the following years, thanks to preventive measures, mainly vaccinations, the incidence of people decreased, and in 1967-1976. it amounted to about 125 infections annually. In the United States, 161 cases were recorded during this period.

Geographical characteristic

Tularemia natural foci are located mainly in regions of the northern hemisphere with a temperate climate. To the south, they are recorded in Mexico, Venezuela, and in the North - beyond the Arctic Circle. In Europe, tularemia is found everywhere in most countries, in Asia - in Iran, Turkey, China, Mongolia and Japan; on the American continent - in Mexico, Venezuela, the USA and Canada.

Epidemiology

Sources of infection from among vertebrates in natural conditions are rodents and hares. In the Soviet Union, the natural reservoir of the pathogen has been found in wild vertebrates (82 species). All animals according to the degree of susceptibility and sensitivity to tularemia are divided into three groups. It is created by some small mammals that are especially susceptible to this disease (mammals of group I): vole, house mouse, muskrat, hare, hamster, etc. The internal organs, blood and secretions of sick or dead mammals have many tularemia microorganisms.

Mammals of group II are small animals (ground squirrel, squirrel, rats, field mouse, Far Eastern voles), which are less susceptible to the disease.

Mammals of the III group - the least susceptible to this disease are carnivores: a fox, a raccoon dog, a ferret, from domestic ones - a cat and a dog. They are practically irrelevant as sources of the tularemia pathogen.

The transmission of this pathogen among mammals is carried out by transmissible arthropods, especially ixodid ticks, mosquitoes, and to a lesser extent fleas and gamasid mites. Along with the blood route, a secondary role is played by food, contact infection (skin and mucous membranes), with the help of water, into which the secretions of an infected animal have fallen.

Pathogenesis

In the development of the infectious process, the following stages are determined: penetration and primary adaptation of the microorganism, spread with the help of lymph, primary regional-focal and general reaction of the body, spread and generalization with blood, secondary foci, changes of a reactive-allergic nature, reverse transformation and the process of recovery. At the site of its penetration, a primary process often develops with regional lymphadenitis or bubo. Inflammation around the lymph node is moderately expressed. The pathogen and its toxins enter the bloodstream, which leads to bacteremia and the spread of the process and the development of secondary foci.

Tularemia: symptoms

The incubation period lasts from 1 to 14 days. The disease has an acute onset, patients often note even a clear time of onset. Chills and fever appear, the temperature rises to 38-40 degrees C. The patient complains of pain in the head, weakness, dizziness, muscle pain, lack of appetite, vomiting. The eyes and skin of the face are red. In severe cases, there is a delusional state, agitation, lethargy is extremely rare. Depending on the clinical forms, there are eye pains, pains when swallowing, retrosternal pains, pains at the site of bubo development. The initial period is characterized by local changes associated with the entrance gate. Without antibiotic therapy, fever lasts up to two to three weeks. Diseases of a protracted and chronic form can take several months. By the end of the first week, the liver and spleen are enlarged. The incubation period in its duration depends on the individual state of the immune system.

Tularemia - what is it? In the clinical picture, the following forms of the course are noted:

Skin-bubonic. This is the most common form - in 50-70% of cases.

Oculobubonic. This form is rarely recorded - in 1-2% of cases.

Anginal-bubonic. Fixed at 1%.

Abdominal.

Pulmonary.

Generalized (typhoid, septic). This form is the most difficult to diagnose.

Subject to differential diagnosis of the disease with a characteristic enlargement of the lymph nodes and tularemia, the symptoms of which can copy other similar diseases, and not only infectious ones. This is a cat scratch disease, which is characterized by the presence of primary affect and regional lymphadenitis with an increase in the lymph node and frequent suppuration.

Complications develop in the form of meningitis, meningoencephalitis, lung abscesses, pericarditis, peritonitis. However, cases of exacerbation and relapse are recorded.

Treatment

It should be noted that tularemia is treated only in the conditions of an infectious diseases hospital. What is it and how is this process carried out? The drugs for tularemia are antibiotics. The skin-bubonic form is not dangerous to humans and can go away spontaneously, however, etiotropic therapy can speed up the healing process. The pulmonary form requires complex treatment with mandatory monitoring of the patient's condition by specialists, since it can lead to sad consequences, up to death. In the case of a chronic course, complex therapy with antibiotics and a vaccine is used. A killed vaccine is used, administered in various ways at a dose of 1-15 million microorganisms at intervals of 3-6 days, the course of therapy is 6-10 injections.

Prevention

In natural foci, they control rodents and ticks. Fishing for hares, water rats, hamsters, etc. reduces the population of animals and prevents the occurrence of epizootics.

Prevention of tularemia provides for: sanitary supervision of a water supply source, food facility, warehouses and housing, preventing rodents from entering them, vaccinating people who have been exposed to possible infection.

Sanitary-educational work among the population is of great importance.

In case of an epizootic, the unvaccinated population is vaccinated. Deratization is carried out in residential buildings, warehouses, catering establishments. In case of transmissible infection, quarantine is established to visit the alleged place of infection of people, extermination of blood-sucking insects is carried out, insect repellent drugs are used - repellents, PPE, Pavlovsky nets, etc. When people are infected in the fishery, when harvesting rodent skins, control over compliance with sanitary veterinary requirements. With a water outbreak of tularemia, the use of water from a seeded source is immediately stopped, the wells are disinfected.

Specific prophylaxis of tularemia, or vaccination, is an effective method of preventing the disease. The tularemia vaccine was developed by N. A. Gaisky and B. Ya. Elbert. Live dry skin vaccination against tularemia is available in ampoules in lyophilized form, it is suitable for long-term storage. In enzootic areas, vaccination is carried out as a planned event.

There is an associated vaccine against tularemia and brucellosis, as well as tularemia and other infections. The immune level of the vaccinated is assessed by the allergic response after a tularin skin test. Timely vaccination of the population in the outbreaks in combination with other preventive measures led to a tangible result, a sharp decrease in the incidence was noted. Currently, only sporadic cases are recorded.

At the present stage, tularemia is one of the most dangerous infections. What it is? This question is asked by medical scientists, since this infection is of interest because of its pronounced natural focality and insufficient knowledge.