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What is the tularemia test for? Antigenic structure of bacteria. Tularemia with damage to internal organs

Tularemia is a natural focal disease that manifests itself as an acute infection. Tularemia, the symptoms of which are the defeat of the lymph nodes and skin, and in some cases the mucous membranes of the pharynx, eyes and lungs, is also distinguished by the symptoms of general intoxication.

general description

The causative agent of the disease is Francisella tularensis, a gram-negative aerobic rod bacterium. It is noteworthy that the tularemia bacillus is an extremely tenacious microorganism, and its viability in water is possible at a temperature corresponding to 4 ° C for about a month. In grain and straw, if the temperature corresponds to zero, the viability of the microorganism can be about six months, at 20-30 degrees the survival of the microorganism is possible for 20 days, and in the skins of animals that died from tularemia, the bacterium can live up to a month at a temperature of 8-12 degrees. The death of bacteria occurs when exposed to high temperatures, as well as disinfectants.

As a reservoir of infection, as well as its source, birds and wild rodents, including some species of mammals (sheep, dogs, lagomorphs, etc.) act. The most significant contribution to the spread of this infection is noted for rodents (muskrat, vole, etc.). As for a person as a distributor of infection, he is not contagious.

In the transmission of bacteria, the most common is the transmission mechanism. In this case, the microbe enters the body of the animal through the bite of a blood-sucking or tick. A characteristic route of infection for the disease is infection through the bite of an ixodid tick.

Considering the prevalence of tularemia, it should be noted that susceptibility to this disease is 100%. For the most part, susceptibility to infection is noted among men, and those of them whose profession predisposes to direct contact with animals. Territorial foci are formed during the migration of infected rodents. Tularemia is mainly relevant for countryside However, in recent years there has been a clear trend towards an increase in the incidence in urban areas.

A different degree of increase in the incidence is observed year-round, while for each season, the manifestation of the disease in its specific form is characteristic. This is explained by etiological factors. A significant number of episodes of morbidity is observed in autumn period meanwhile, transmissible outbreaks of tularemia associated with haymaking and harvesting in the fields often occur in the period of July-August.

Features of the transmission of the causative agent of tularemia

Below is a diagram indicating the features of the transmission of the disease, depending on the metamorphic development of the tick.


The number "1" indicates infection of tick larvae through small mammals with tularemia. The number "2" determines the next cycle, in which the nymphs that have molted from the larvae carry out the transmission of the pathogen to small mammals. "3" indicates the transmission of the causative agent of infection by mature ticks that have molted from nymphs to large mammals.

The course of tularemia

The penetration of the pathogen occurs through the skin, even if it is not damaged. As we have already indicated, mucous membranes become sites for penetration. respiratory tract and eyes, as well as the gastrointestinal tract.

The area of ​​the so-called entrance gate largely determines clinical features course of tularemia. Often in this area there is a development of a primary affect, in which the sequence of succession of spots, papules, vesicles, pustules and ulcers becomes relevant. Somewhat later, tularemia bacilli enter the region of regional lymph nodes, in which their subsequent reproduction occurs with the simultaneous development of the inflammatory process. It should be noted that the inflammatory process is accompanied by the formation of a primary bubo (that is, an inflamed lymph node). The death of Francisella leads to the release of the lipopolysaccharide complex (endotoxin), which, in turn, enhances local inflammation and provokes the development of intoxication when it enters the bloodstream.

With hematogenous dissemination, generalized forms of infection develop, occurring with characteristic toxic-allergic manifestations. In addition, secondary buboes are also formed, various systems and organs are affected (in particular, the lungs, spleen and liver). In the area of ​​the lymph nodes, as well as the internal organs that have been affected, a specific type of granuloma is formed in combination with central areas with necrosis. There is also an accumulation of granulocytes, lymphoid and epithelial elements.

The incomplete process of phagocytosis predisposes to the formation of granulomas, which is due to the peculiarities of the properties of the pathogen (in particular, factors that prevent killing inside cells are isolated here). Often, the formation of granulomas in primary buboes leads to the formation of suppuration in them, followed by spontaneous opening. A similar course of the process is characterized by prolonged healing of the resulting ulcer.

As for the secondary buboes, for them, as a rule, suppuration is not a characteristic feature. When replacing necrotic areas that have arisen in the lymph nodes with connective tissue, suppuration does not occur, while buboes are sclerosed or absorbed.

Forms of tularemia

The clinical classification of the disease in question distinguishes the following forms:

  • According to the localization of the local process:
    • Tularemia bubonic;
    • Tularemia ulcerative bubonic;
    • Tularemia oculo-bubonic;
    • Tularemia anginal-bubonic;
    • Tularemia pulmonary;
    • Tularemia abdominal;
    • Tularemia is generalized.
  • Depending on the duration of the course of the disease:
    • Acute tularemia;
    • Protracted tularemia;
    • Recurrent tularemia.
  • Depending on the severity of the course:
    • Tularemia is mild;
    • Tularemia is moderate;
    • Tularemia is severe.

Tularemia: symptoms

Duration incubation period is about 1-30 days, but most often - 3-7 days.

General signs characteristic of tularemia, and, accordingly, signs characteristic of any of its clinical forms, are manifested in an increase in temperature (up to 40 ° C) and in symptoms indicating intoxication (headache, muscle pain, chills, weakness, anorexia - lack of appetite, in which it is noted complete absence). Most often, fever has a relapsing character, as well as a constant, undulating, or intermittent character. The duration of the fever can be about a week, but it can also last for two to three months. Meanwhile, mainly its duration varies within three weeks.

Examination of patients indicates hyperemia and general pastosity of the face (that is, whitening of the skin in combination with loss of elasticity caused by mild edema), hyperemia (redness) of the conjunctiva is also observed. In frequent cases, the appearance of an exanthema of a particular nature (maculopapular, erythematous, vesicular, roseolous or petechial) becomes possible. The pulse is rare, the pressure is low. After a few days from the onset of the disease, the development of hepatolienal syndrome is noted.

It should be noted that the development of one or another clinical form of tularemia is determined based on the mechanism of infection, as well as the entrance gate of infection, which, as we noted, indicate the local localization of the process. From the moment of penetration through the skin of the pathogen, the development of bubonic form s disease, which manifests itself, respectively, in the form of lymphadenitis (bubo), regional in relation to the gate of infection. Lymphadenitis implies, in particular, inflammation of the lymph nodes.

In addition, a combined or isolated lesion becomes possible, which affects various groups of lymph nodes (inguinal, axillary, femoral). Hematogenous dissemination of pathogens can also contribute to the formation of secondary buboes. This is accompanied by soreness and subsequent enlargement of the lymph nodes, which can reach the size of a hazelnut or a small chicken egg. Gradually, pain reactions in their manifestations decrease, then completely disappear. The contours characteristic of the bubo do not lose their distinctness, slight manifestations of periadenitis are noted. The dynamics of tularemia is characterized by slow resorption and suppuration with the appearance of a fistula, this is accompanied by the release of creamy pus.

Ulcerative bubonic form. Predominantly, the development of this form occurs in the case of transmissible infection. The place where the introduction of the microorganism occurred, for several days is characterized by the successive replacement of each other by such formations as a spot and a papule, a vesicle and a pustule, after which a shallow ulcer with slightly raised edges is formed. Its bottom is covered with a dark crust, in shape it resembles a “cockade”. In parallel with this, the development of regional lymphadenitis (bubo) also occurs. In the future, the ulcer scars at an extremely slow pace.

When a bacterium enters the conjunctiva, it forms oculo-bubonic form diseases. This is accompanied by damage to the mucous membranes of the eye, which occurs according to the principle of conjunctivitis, papular-type formations, and after - formations of an erosive-ulcerative type when yellowish pus is released from them. The process of corneal damage in this case is an extremely rare phenomenon. This symptomatology is accompanied by the severity of eyelid edema, as well as regional lymphadenitis. The severity and duration of the course of the disease are noted.

Anginal-bubonic form. Its development occurs when the pathogen penetrates through water or food. There are complaints from patients on manifestations in the form of moderate pain in the throat, difficulty swallowing. Inspection reveals hyperemia of the tonsils, their increase in size, swelling. In addition, they are soldered to the fiber surrounding them. The surface of the tonsils (mainly on one side) is covered with a grayish-white necrotic coating, which is difficult to remove. There is a pronounced swelling of the tongue and arches. With the course of the disease, the tissues of the affected tonsil are destroyed during the formation of long-term healing and rather deep ulcers. The concentration of tularemia buboes covers the cervical, parotid and submandibular regions, which basically corresponds to the side of the tonsil lesion.

Abdominal form. Its development occurs due to lesions in the mesenteric lymph nodes. Symptoms are manifested in the occurrence of severe pain in the abdomen, in some cases - vomiting and anorexia. Diarrhea has also been noted in some cases. Palpation determines soreness in the navel, does not exclude symptoms indicating irritation of the peritoneum. In addition to these symptoms, hepatolienal syndrome also occurs. Palpation of the mesenteric lymph nodes is possible in rare cases, their increase is determined using such an examination method as ultrasound.

Lung form. Its course is possible in a bronchitis or pneumonic variant.

  • Bronchial flow. This variant is caused by the defeat of the paratracheal, mediastinal and bronchial lymph nodes. It is characterized by moderate intoxication and dry cough, pain in the retrosternal region. Dry rales are noted when listening to the lungs. As a rule, this course is characterized by its own ease, while recovery occurs within 10-12 days.
  • Pneumonic flow. It is characterized by an acute onset, the course of the disease in this form is debilitating and sluggish, for a long time concomitant symptom fever appears. The pathology formed in the lungs has manifestations in the form of focal pneumonia. Pneumonia is distinguished by the severity and acyclicity of its course, as well as a tendency to the subsequent development of complications (segmental, lobular or disseminated pneumonia with a characteristic increase in the lymph nodes of one or another of the listed groups, as well as pleurisy and cavities, including lung gangrene).

The form is generalized. Her clinical manifestations similar to typhoid-paratyphoid infections or severe. Fever is characterized by the intensity of its manifestations and its long-term persistence. Symptoms of intoxication (chills, headache, weakness, muscle pain) also become pronounced. There is lability (variability) of the pulse, deafness of heart sounds, low pressure. In the vast majority of cases, the first days of the disease proceed with the development of hepatolienal syndrome. Subsequently, it becomes possible to form an exanthema of a persistent roseolous petechial character with the localization of the elements characteristic of the rash in the area of ​​\u200b\u200bsymmetric parts of the body (hands, forearms, feet, lower legs, etc.). This form does not exclude the possibility of developing secondary buboes, which are caused by the dissemination (spread) of the pathogen, as well as the dissemination of specific metastatic pneumonia.

Complications of tularemia

Mostly, their relevance can be discussed in the case of the development of a generalized form. Most often, tularemia pneumonia of the secondary type occurs, often a shock of an infectious-toxic nature is formed. Rare cases are marked by the occurrence of myocarditis, meningoencephalitis, and other pathologies.

Diagnosis of tularemia

The use of non-specific laboratory techniques (,), determines the presence of signs characteristic of inflammation and intoxication. The disease in the first days of its course manifests itself in neutrophilic leukocytosis in the blood, then a drop in the total number is observed. Simultaneously with this increase is subjected to the concentration of fractions of monocytes and lymphocytes.

Serological specific type of diagnosis is carried out using RNGA and RA. The progression of the disease is characterized by an increase in antibody titer. Determination of tularemia becomes possible already on the 6-10th day from the moment of its onset, for which immunofluorescent analysis (ELISA) is used. This serological test in relation to the diagnosis of tularemia is characterized by the greatest sensitivity. As for the possibility of earlier diagnosis of the disease (its first days), it is possible with the help of PCR.

A very specific and, at the same time, fast diagnostics is carried out using skin allergy test, which is produced using tularemic toxin. The result is determined already by the 3-5th day of the disease.

Treatment of tularemia

Treatment of tularemia is carried out exclusively in a hospital, while discharge is made only when complete cure from the disease. Specific therapy is used in the form of a course of antibiotics. The removal of intoxication symptoms is carried out using therapy oriented in this direction in combination with antipyretic and anti-inflammatory medications. Additionally assigned antihistamines and vitamins. In some cases, if necessary, drugs are also used to normalize cardiovascular activity.

Tularemia I Tularemia (tularaemia; Tulare name of the area in California + Greek haima)

Immunity. In those who have been ill, a persistent one is formed. With the introduction of live tularemia, artificial immunity is achieved, which lasts up to 5 years or more.

Clinical picture. There are bubonic, ulcerative-bubonic, oculobubonic, anginal-bubonic, abdominal, pulmonary and generalized forms of T. A number of manifestations of the disease are characteristic of all forms. lasts several hours up to 3 weeks, on average 3-7 days. begins suddenly with chills and a rapid rise in temperature to 38-40 °, there are sharp, dizziness, in the muscles (especially in the calf), lack of appetite, sleep disturbance, and sometimes nausea. Fever is often relapsing type, lasting from several days to 2 months. and more, more often 2-3 weeks. edematous, face and conjunctiva are hyperemic, vessels are injected. On the mucous membrane of the oral cavity, petechial hemorrhages are visible, lined. From the 3rd day of the disease, a variety of diseases can appear on the skin, followed by peeling and pigmentation. Typical enlargement of various lymph nodes. From the 2-3rd day of the disease, the spleen increases, from the 6-9th. Moderate or severe leukocytosis, relative lymphomonocytosis, and an increase in ESR are found in the blood.

In the bubonic form, after 2-3 days from the onset of the disease, an increase in one or another group of lymph nodes (axillary, femoral, inguinal, etc., rice. 1 ). Buboes are moderately painful, have clear contours, size - from 1 to 5 cm; resolve slowly with alternating periods of improvement and exacerbation. In cases of suppuration, the opening of the buboes occurs after 2-4 weeks. with the formation of a fistula, the release of thick pus, further scarring and sclerosis.

In the ulcerative-bubonic form, simultaneously with an increase in body temperature, primary inflammatory changes develop in the form of a spot at the site of the introduction of the pathogen, then papules, vesicles, pustules and ulcers. shallow, regular round shape, its bottom is covered with serous-purulent discharge; it is a little painful, heals slowly with the formation of an atrophic scar. In the regional lymph nodes, the same changes are noted as in the bubonic form.

The oculobubo form is characterized by anterior cervical submandibular or parotid lymphadenitis, damage to the eyes (usually one). There is a sharp swelling of the eyelid, often with ulcers and yellow follicles.

With anginal-bubonic form, patients complain of sore throat, difficulty in swallowing. enlarged, often on one side, covered with a grayish-white coating. Subsequently, deep, slowly healing ulcers form. Simultaneously with angina, a submandibular or cervical bubo occurs ( rice. 2 ).

The abdominal form is characterized by lymph nodes of the mesentery of the intestine. typical cramping pains in a stomach. Nausea, vomiting, stool retention may occur, sometimes. On palpation, it is noted in the middle part of the abdomen. The pulmonary form occurs with damage to the bronchi and trachea (bronchitis variant) or lungs (pneumonic variant). In the first case, there is dry, pain behind the sternum, scattered dry. After 11-12 days, the disease ends with recovery. The pneumonic variant is characterized by a severe and prolonged course with a tendency to relapse, the development of abscesses, bronchiectasis, pleurisy, etc. Patients complain of chest pain, dry, rarely wet cough. Dry, finely bubbling wet rales are heard in the lungs. At x-ray examination from the end of the first week of the disease, inflammatory changes in the lungs, enlarged hilar, paratracheal and mediastinal lymph nodes are detected.

The generalized form is characterized by the development of severe toxicosis without local changes, weakness, severe headaches and muscle pain; sometimes loss of consciousness is possible. The fever is undulating, lasts up to 3 weeks. and more. On the skin of the limbs or face, neck, chest, symmetrical rashes often appear, initially pink-red, then cyanotic. The rash lasts 8-12 days. In some patients, swelling of the joints of the hands or feet is noted. slow, relapses are possible.

Diagnosis is based on epidemiological (stay in the natural focus of T., contact with sick animals, bites of blood-sucking arthropods, etc.) and clinical data. To confirm the diagnosis, a skin allergy test and laboratory data are used. An allergic test is carried out by intradermal injection of 0, ml tularemia antigen - gularin. She's estimated in 24-48 h and is considered positive for hyperemia and infiltrate with a diameter of at least 0.5 cm. The test becomes positive from the 3-5th day of illness and persists for many years. Possible positive reactions in persons vaccinated against T. is based on the results of serological studies (agglutination reactions or passive hemagglutination, etc.). Differential is primarily carried out with the bubonic form of plague in the territory of natural foci of these infections. With plague, it is more pronounced, characterized by sharp soreness and the absence of clear contours of the bubo.

Treatment. Patients are hospitalized, streptomycin is prescribed, chloramphenicol and tetracycline drugs are less effective. Enter water-electrolyte, glucose solutions, hemodez, polyglucin, etc.), antihistamines (diphenhydramine, pipolfen, etc.), (C and group B). Heat is shown locally on the bubo, during fluctuations, a wide one is produced, the obsessed bubo is emptied and necrotic masses are removed. In the anginal-bubonic form, throats are prescribed with antiseptic solutions, with eye damage - albucid-sodium, antibiotic ointments.

Forecast favorable. Lethal outcomes observed rarely, mainly in pulmonary and abdominal forms.

Prevention. In natural foci of T., they fight against rodents (see Deratization) and blood-sucking arthropods (see Disinsection) , systematically control the number of rodents. In settlements where T. is common, they control the sanitary condition of water supply sources, dwellings, shops, warehouses, etc., do not allow rodents to enter them, and prohibit drinking water from open reservoirs and swimming in them. Persons trapping rodents and processing their skins should use protective clothing (overalls, rubber apron, gloves, goggles, cotton-gauze masks). In cases of an epizootic among rodents page - x. workers are also advised to wear cotton-gauze masks when stacking hay, straw, threshing bread, etc. Apply from the attack of blood-sucking arthropods - protective clothing. They carry out sanitary and educational work, explain measures to prevent infection with T. Persons living in the territory of natural foci, traveling to them for seasonal work, tourists, as well as persons most at risk of infection due to their profession, are given specific prophylaxis (vaccination) of live tularemia dry cotton. At emergence in the center of T. of a disease among people of all not vaccinated vaccinate.

Bibliography: Guide to zoonoses, ed. IN AND. Pokrovsky, p. 225, L., 1983; Guide to infectious diseases, ed. IN AND. Pokrovsky and K.M. Loban, p. 285, M, 1986.

A patient with an anginal-bubonic form of tularemia: enlarged submandibular lymph nodes are visible on the right">

Rice. 2. A patient with anginal-bubonic form of tularemia: enlarged submandibular lymph nodes are visible on the right.

II Tularemia (tularaemia; Tulare name of the area in California + Greek haima blood; .: hare disease, mouse disease, deer fly fever, small plague)

acute infectious natural focal disease from the group of bacterial zoonoses caused by Francisella tularensis; transmitted to a person by contact, alimentary, airborne or transmissible way.

Tularemia abdominal(t. abdominalis; synonym T. intestinal) - the clinical form of T., which occurs when the pathogen is introduced through the mucous membrane gastrointestinal tract, less often as other forms of the disease; characterized by damage to the mesenteric lymph nodes, the formation of erosions and ulcers along the intestine.

Tularemia anginal-bubonic(t. anginosobubonica) - the clinical form of T., which occurs when the pathogen is introduced through; characterized more often by one-sided lesion with the formation of deep ulcers, raids and regional buboes.

Tularemia bubonic(t. bubonica) - the clinical form of T., arising from a transmissible or contact route of infection; characterized by regional lymphadenitis and the formation of buboes containing the pathogen.

Tularemia generalized(t. generalisata; synonym: T. septic, T. typhoid) is a clinical form of T., characterized by bacteremia, severe intoxication with symptoms resembling or sepsis, and differing from it by the absence of primary affect and regional bubo.

Tularemia oculobubonic(t. oculobubonica; syn. T. oculo-glandular) - a variant of bubonic T., which occurs when the pathogen enters through the conjunctiva, characterized by the development of conjunctivitis, sometimes with the formation of papules and sores and swelling of the eyelids.

Tularemia oculoglandular(t. oculoglandularis) - see Tularemia oculobubonic.

Tularemia intestinal- see Tularemia abdominal.

Tularemia pulmonary secondary(t. pulmonalis secundaria) is a clinical form of T. that occurs when a pathogen enters the lungs or bronchopulmonary lymph nodes with blood or lymph and is characterized by the development of multiple inflammatory foci in them.

- natural focal acute infection that affects the lymph nodes, skin, sometimes the mucous membranes of the eyes, throat and lungs. Tularemia occurs with severe symptoms of general intoxication, prolonged fever, generalized lymphadenitis, hepatosplenomegaly, polymorphic rash and other symptoms. Specific diagnosis of tularemia is carried out using serological reactions (ELISA, RA, RNGA), PCR, skin-allergic tests. In the treatment of tularemia, antibacterial, detoxification therapy, surgical opening and drainage of festering buboes are used.

ICD-10

A21

General information

Tularemia - acute bacterial infection, flowing with a febrile syndrome, specific lymphadenitis and polymorphic manifestations due to the entrance gate. Depending on the method of infection, bubonic, ulcerative-bubonic, oculobubonic, anginal-bubonic, pulmonary, abdominal and generalized forms of tularemia are distinguished. Foci of tularemia are found in many countries of the northern hemisphere; in Russia they are located mainly on the territory of the European part and Western Siberia. Along with plague, cholera, anthrax and other infections, tularemia is classified as a particularly dangerous infection.

Clinical classification of tularemia is made depending on the location of the infection (bubonic, ulcerative-bubonic, oculobubonic, angio-bubonic, abdominal and generalized tularemia), duration (acute, protracted and recurrent) and severity (mild, moderate and severe).

Exciter characteristic

The causative agent of tularemia is the aerobic Gram-negative rod bacterium Francisella tularensis. The tularemia bacillus is a fairly tenacious microorganism. It remains viable in water at a temperature of 4 ° C for up to a month, on straw or in grain at zero temperature for up to six months, a temperature of 20-30 ° C allows bacteria to survive for 20 days, and in the skins of animals that died from tularemia, the microorganism persists for about a month at 8- 12 degrees. Bacteria die when exposed to high temperatures and disinfectants.

The reservoir of infection and its source are wild rodents, birds, some mammals (hare-like, dogs, sheep, etc.). The greatest contribution to the spread of infection is made by rodents (voles, muskrats, etc.). A sick person is not contagious. The most common transmission mechanism. The microbe enters the body of animals with the bite of a tick or blood-sucking insects. Tularemia is characterized by infection of animals when bitten by an ixodid tick. A person becomes infected by contact with sick animals (skinning, collecting rodents) or by eating food and water infected by animals.

The respiratory route of infection is realized by inhalation of dust from grain or straw contaminated with bacteria, in agricultural production (processing of vegetable raw materials, meat processing plants, slaughter of large cattle and etc.). Despite the low probability of infection with tularemia outside the natural focus of the pathogen, it is possible to get sick through contact with products and raw materials imported from epidemiologically disadvantaged areas. Human susceptibility to tularemia is extremely high, the disease develops in almost 100% of those infected.

Symptoms of tularemia

The incubation period of tularemia can range from one day to a month, but is most often 3-7 days. Tularemia of any localization usually begins with an increase in body temperature to 38-40 degrees, the development of intoxication, manifested by weakness, muscle pain, headache. Fever is most often remittent, but may be constant, intermittent, or undulating (two to three waves). The duration of the fever can range from a week to two to three months, but is usually 2 to 3 weeks.

On examination, there is hyperemia of the face, conjunctiva and mucous membranes. oral cavity, nasopharynx, pastosity, sclera injection. In some cases, exanthema (skin rash) of various types is found. Bradycardia, low blood pressure. A few days after the onset of fever, hepatosplenomegaly appears.

The variety of clinical forms of tularemia is associated with the mode of infection. In the event that the skin serves as the entrance gate of infection, a bubonic form develops, which is a regional lymphadenitis. Axillary, inguinal, femoral lymph nodes can be affected, with further spread, secondary buboes may be noted.

The affected lymph nodes are enlarged (sometimes reaching the size of a chicken egg), with distinct contours, initially painful, then the pain decreases and subsides. Gradually, the buboes resolve (often within several months), sclerosis or suppurate, forming abscesses, which then open onto the skin with the formation of a fistula.

The ulcerative-bubonic form usually develops with transmissible infection. At the site of the introduction of microorganisms, an ulcer is formed (bypassing successively the stages of spots, papules, vesicles and pustules) with raised edges and a bottom covered with a dark crust, of small depth, resembling a cockade. The ulcer heals extremely slowly. In parallel, regional lymphadenitis develops.

When the pathogen penetrates through the conjunctiva, tularemia manifests itself in the form of an oculobubonic form: a combination of ulcerative-purulent conjunctivitis with regional lymphadenitis. Conjunctivitis manifests itself in the form of inflammation (redness, swelling, soreness, a feeling of sand in the eyes), then papular formations appear, progressing in erosion and ulcers with purulent discharge. The cornea is usually not affected. This form of tularemia is often very difficult and prolonged.

The anginal-bubonic form occurs if the pharyngeal mucosa serves as the gate of infection, infection occurs through the use of contaminated food and water. Clinically manifested by sore throat, dysphagia (difficulty swallowing), on examination, hyperemia and swelling of the tonsils are noted. On the surface of the enlarged, soldered to the surrounding tissue, tonsils are often visible grayish, hard to remove necrotic plaque. As the disease progresses, the tonsils become necrotic, forming hard-to-heal ulcers and, later, scars. Lymphadenitis in this form of tularemia occurs in the parotid, cervical and submandibular nodes from the side of the affected tonsil.

When infected with an infection lymphatic vessels mesentery of the intestine tularemia manifests itself in the form of an abdominal clinical form, severe abdominal pain, nausea (sometimes vomiting), anorexia. Diarrhea may occur. Palpation tenderness is localized in the umbilical region, hepatosplenomegaly is noted.

The pulmonary form of tularemia (developing by inhalation of dust containing bacteria) occurs in two clinical variants: bronchitis and pneumonia. Bronchitis variant (with the defeat of the bronchial, paratracheal mediastinal lymph nodes) is characterized by a dry cough, moderate pain behind the sternum and general intoxication, proceeds quite easily, recovery usually occurs in 10-12 days. The pneumonic form proceeds for a long time, the onset is gradual, the course is debilitating with signs of focal pneumonia. Pneumonic tularemia is often complicated by bronchiectasis, pleurisy, abscess formation, caverns, up to pulmonary gangrene.

The generalized form proceeds according to the type of typhoid and paratyphoid infections or sepsis. Fever incorrectly remitting, long-lasting, severe intoxication, intense muscle pain, progressive weakness, headache, dizziness, delirium, hallucinations, confusion.

Complications of tularemia

Complications of tularemia are characteristic of its generalized form; one of the most common complications is secondary pneumonia. With the generalization of infection, the development of infectious-toxic shock is possible. Sometimes tularemia can be complicated by meningitis and meningoencephalitis, inflammation of the heart sac, arthritis.

Diagnosis of tularemia

Nonspecific laboratory methods (general blood count, urine) show signs of inflammation and intoxication. In the first days of the disease in the blood, neutrophilic leukocytosis, then the total number of leukocytes falls, the concentration of fractions of lymphocytes and monocytes increases.

Specific serological diagnosis is made using RA and RNHA (direct agglutination and indirect hemagglutination reactions). With the progression of the disease, an increase in the titer of specific antibodies occurs. From 6-10 days after the onset of the disease, it is possible to determine tularemia using immunofluorescence assay (ELISA) - the most sensitive serological test for tularemia. For early diagnosis (in the first days of fever), PCR can be used. A quick and rather specific diagnosis can be carried out using a skin-allergic test with tularemic toxin (it gives a result already on the 3rd-5th day of illness).

Since the isolation of bacteria from the blood and other biological materials presents a certain difficulty, bacteriological culture is rarely carried out. On the 7-10th day of the disease, the pathogen can be isolated by culture of discharged ulcers, punctate of buboes, but the laboratory tools necessary for sowing this culture are not very common. In the pulmonary form of tularemia, an x-ray or CT scan of the lungs is performed.

Treatment of tularemia

Tularemia is treated in a hospital with an infectious profile, and discharge is made after complete recovery. Specific Therapy tularemia is to prescribe a course of antibiotics: streptomycin with gentomycin intramuscularly. In addition, other antibiotics can be used a wide range(doxycycline, kanamycin). If the drugs of choice are ineffective, second-line antibiotics (third-generation cephalosporins, chloramphenicol, rifampicin) are prescribed.

To relieve the symptoms of intoxication, detoxification therapy is performed (with severe intoxication intravenous infusion solutions for detoxification), anti-inflammatory and antipyretic drugs (salicylates) and antihistamines, vitamins. If necessary - cardiovascular drugs. Skin ulcers cover sterile dressings, festering buboes are opened and drained.

Prevention of tularemia

Prevention of tularemia includes measures to disinfect sources of distribution, suppression of transmission routes. Of particular importance in preventive measures is the sanitary and hygienic state of food and agriculture enterprises in areas endemic for this pathogen, deratization and disinsection.

Individual protection measures against infection are necessary when hunting wild animals (skinning, butchering), deratization (when collecting poisoned rodents). It is desirable to protect hands with gloves, or thoroughly disinfect after contact with animals. In order to suppress the alimentary route of transmission, it is desirable to avoid drinking water from an unreliable source without special treatment.

Specific prophylaxis of tularemia is the vaccination of the population in endemic areas with a live tularemia vaccine. Immunity is formed for 5 or more (up to seven) years. Revaccination after 5 years. emergency prophylaxis (for high probability infection) is carried out with the help of intravenous administration of antibiotics. When a patient with tularemia is identified, only those things that were used in contact with an animal or infected raw materials are subject to disinfection.

Tularemia is infectious disease, which is characterized by natural focality, causes inflammatory processes at the site of penetration of pathogens, regional lymphadenitis, fever and general intoxication of the body. The causative agent of tularemia is able to persist for a long time in adverse conditions, therefore, if left untreated, the disease is prone to a protracted course and development into a chronic form.

In places where tularemia is common, vaccination is mandatory for the entire population, with the exception of children under 7 years of age and those who have contraindications to the vaccine. The first vaccination is a single dose, re-vaccination is carried out every 5 years. As for the definition of unfavorable regions. These include areas where cases of tularemia infection have been reported, or areas where tularemia antigens are regularly isolated from objects. external environment. In other cases, vaccination of the population concerns only persons belonging to risk groups.

What happens when a pathogen enters the body?

The main sources of tularemia are water rats, mice, hares and other rodents. Sick people do not pose a danger, that is, if you are diagnosed with tularemia, the symptoms of the disease should only concern you. Your family members, work colleagues and close friends are not at risk of tularemia. You can catch tularemia in cases where bacteria gain access to the inside of the body through scratches and other damage to the skin or mucous membranes. Another common route of infection is drinking water contaminated by rodents.

Immediately after entering the human body, the tularemia pathogen begins to multiply intensively and, sooner or later, the bacteria spread to all organs and systems. They settle mainly in the lymph nodes, liver, spleen and lungs. If tularemia begins to develop, symptoms usually appear after 3-6 days. Patients suddenly have a fever, muscle pain, nausea, and headache. Note that the temperature often reaches critical levels, therefore, with a diagnosis of tularemia, treatment should begin immediately after the correct diagnosis is made.

Clinical picture of tularemia

The characteristic features of tularemia largely depend on how exactly the bacteria entered the body. The most common form of infection is bubonic tularemia, which develops as a result of skin lesions. We list the most obvious symptoms of tularemia:

  • the appearance of festering ulcers at the site of penetration of bacteria;
  • constant itching in the area of ​​damaged skin;
  • swollen lymph nodes (can reach a diameter of 5-9 cm);
  • suppuration of the lymphatic nodes, followed by rupture of the focus and the release of thick, creamy pus.

In some cases, pustules resolve on their own, but we do not advise you to wait for “weather by the sea”, because the process of self-liquidation is very long, and ulcers look quite unpleasant and significantly reduce the quality of human life. In addition, cutaneous tularemia, the diagnosis of which is not special problems well responds to treatment. This is another strong argument in favor of not postponing a visit to the doctor.

A few words about other forms of tularemia:

  • oculobubonic tularemia - develops due to the penetration of pathogens into the conjunctiva of the eye;
  • angio-bubonic form - due to the ingress of bacteria into the human mouth. The signs of the disease are similar to a sore throat, but it proceeds much more severely - with high fever, severe fever and a significant increase in the cervical lymph nodes;
  • abdominal tularemia - accompanied by abdominal pain, nausea, vomiting, open intestinal bleeding(may not appear in all patients). In this case, the symptoms of infection are similar to appendicitis, which makes it difficult to make a correct diagnosis;
  • pulmonary form of tularemia - due to the ingress of pathogens into the lungs. The disease is severe, accompanied by severe pain in the chest. If a patient is diagnosed with pulmonary tularemia, vaccination is a mandatory step in treatment, since there is a real possibility of developing serious complications (abscesses) and irreversible deformities of the lungs.

Treatment of tularemia

Antibiotics are the drugs of choice for tularemia. The cutaneous form of tularemia is not dangerous to humans and can go away on its own, but specific treatment allows you to speed up this process, saves a person from contemplating ugly sores. The pulmonary form causes much more dramatic consequences and requires integrated approach with mandatory constant monitoring of the patient's condition.

Prevention of tularemia consists in routine vaccination of the population. The risk group includes people living in floodplains, as well as employees of enterprises specializing in the preparation of skins of muskrat, water rats and hares.

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Tularemia- acute infection natural focal disease with damage to the lymph nodes, skin, sometimes eyes, throat and lungs, and accompanied by severe intoxication.

Brief historical information
In 1910, in the area of ​​​​Lake Tulare in California, D. McCoy discovered a disease in gophers that resembles clinical picture bubonic plague. Soon, he and Ch. Chapin isolated a pathogen from sick animals, which was named Bacterium tularense (1912). Later it was found that people are also susceptible to this infection, and at the suggestion of E. Francis (1921) it was called tularemia. Later, the pathogen was named after Francis, who studied it in detail.

What provokes / Causes of Tularemia

The causative agent is immobile gram-negative aerobic encapsulated bacteria F. tularensis of the genus Francisella of the Brucellaceae family. Show pronounced polymorphism; most often have the form of small coccobacilli.
There are three subspecies of bacteria:
1. Nearctic (African);
2. Central Asian;
3. Holarctic (European-Asian).

The latter includes three biological variants: Japanese biovar, erythromycin-sensitive and erythromycin-resistant. Intraspecific differentiation of the causative agent of tularemia is based on differences in subspecies and biovars in a number of phenotypic traits: biochemical activity, composition of higher fatty acids, the degree of pathogenicity for humans and animals, sensitivity to certain antibiotics, as well as the characteristics of the ecology and the range of the pathogen. Bacteria have O- and Vi-antigens. Bacteria grow on yolk or agar media supplemented with rabbit blood or other nutrients. Of laboratory animals, white mice and guinea pigs are susceptible to infection. Outside the host organism, the pathogen persists for a long time. So, in water at 4 ° C, it remains viable for 1 month, on straw and grain at temperatures below 0 ° C - up to 6 months, at 20-30 ° C - up to 20 days, in the skins of animals that died from tularemia, at 8 -12 "C - more than 1 month. Bacteria are unstable to high temperature and disinfectants. For disinfection, a 5% solution of phenol, a 1:1000 sublimate solution (kills bacteria within 2-5 minutes), 1-2% formalin solution (destroys bacteria in 2 hours), 70 ° ethyl alcohol, etc. are used. For complete disinfection of the corpses of infected animals should be kept for at least 1 day in disinfectant solution and then autoclaved and incinerated.

Epidemiology
Reservoir and source of infection- Numerous species of wild rodents, hares, birds, dogs, etc. Bacteria were isolated from 82 wild species, as well as from domestic animals (sheep, dogs, artiodactyls). The main role in maintaining infection in nature belongs to rodents (water rat, common vole, muskrat, etc.). A sick person is not dangerous to others.

Transfer mechanism- multiple, most often transmissive. The causative agent persists in nature in the “tick-animal” cycle, is transmitted to farm animals and birds by ticks and blood-sucking insects. Specific carriers of tularemia are ixodid ticks. A person becomes infected with tularemia as a result of direct contact with animals (removal of skins, collection of dead rodents, etc.), as well as by the alimentary route through food products and water infected with rodents. Often, infection occurs through blood-sucking vectors (ticks, mosquitoes, fleas, horseflies and other arthropods). Infection is also possible by the respiratory route (by inhalation of infected dust from grain, straw, vegetables). Cases of human diseases have been registered in industries associated with the processing of natural raw materials (sugar, starch-treacle, alcohol, hemp plants, elevators, etc.), in meat processing plants, during the slaughter of sheep and cattle, which had infected ticks, on outskirts of cities located near natural foci. Cases of importation of infection during the transportation of products and raw materials from areas unfavorable for tularemia are known.

natural susceptibility people is high (almost 100%).

Main epidemiological signs. Tularemia is a common natural focal disease that occurs mainly in landscapes of the temperate climate zone. northern hemisphere. Wide use pathogen in nature, involvement in its circulation of a large number of warm-blooded animals and arthropods, contamination of various objects environment(water, food products) also determine the characteristics of the epidemic process. There are different types of foci (forest, steppe, meadow-field, name-bog, in the river valley, etc.). Each type of foci corresponds to its own species of animals and blood-sucking arthropods that take part in the transmission of the pathogen. Adults predominate among the sick; often the incidence is associated with the profession (hunters, fishermen, agricultural workers, etc.). Men get sick 2-3 times more often than women. Anthropurgic foci of tularemia occur during the migration of infected rodents from habitats to settlements where they come into contact with synanthropic rodents. Tularemia remains a disease of rural areas, however, a steady increase in the incidence of the urban population is currently noted. Tularemia is registered throughout the year, but more than 80% of cases occur in summer and autumn. IN last years incidence is sporadic. In some years, local transmissible, commercial, agricultural, water outbreaks are noted, less often outbreaks of other types. Transmissible outbreaks are caused by the transmission of the infectious agent by blood-sucking Diptera and occur in the foci of epizootic tularemia among rodents. Transmissible outbreaks usually begin in July or June, peak in August, and cease in September-October; haymaking and harvesting work contribute to the rise in the incidence.

The industrial type of outbreaks is usually associated with the capture of water rats and muskrats. Commercial flashes occur in spring or early summer during the flood period, and their duration depends on the period of harvesting. Infection occurs through contact with animals or skins; the pathogen penetrates through lesions on the skin, and therefore axillary buboes often occur, often without ulcers at the site of introduction.

Water outbreaks determine the entry of pathogens into open water bodies. The main water pollutant are water voles that live along the banks. Diseases usually occur in the summer with a rise in July. Diseases are associated with field work and the use of drinking water from random reservoirs, wells, etc. In 1989-1999. the proportion of isolates of the causative agent of tularemia from water samples reached 46% or more, which indicates the important epidemiological significance of water bodies as long-term reservoirs of infection.

Agricultural outbreaks occur when airborne dust aerosol is inhaled when working with straw, hay, grain, feed contaminated with the urine of sick rodents. Pulmonary forms predominate, less often abdominal and anginal-bubonic forms. Household type of outbreaks characterizes infection in everyday life (at home, on the estate). Infection is also possible during floor sweeping, sorting and drying agricultural products, distributing feed to pets, and eating contaminated products.

Pathogenesis (what happens?) during Tularemia

Bacteria enter the human body through the skin (even intact), mucous membranes of the eyes, respiratory tract and gastrointestinal tract. In the area of ​​the entrance gate, the localization of which largely determines the clinical form of the disease, the primary affect often develops in the form of successive spots, papules, vesicles, pustules and ulcers. In the future, tularemia sticks enter the regional lymph nodes, where they multiply and develop an inflammatory process with the formation of the so-called primary bubo (inflamed lymph node). With the death of Francisella, a lipopolysaccharide complex (endotoxin) is released, which enhances the local inflammatory process and, when it enters the bloodstream, causes the development of intoxication. Bacteremia does not always occur during the disease. In the case of hematogenous dissemination, generalized forms of infection develop with toxic-allergic reactions, the appearance of secondary buboes, lesions various bodies and systems (primarily the lungs, liver and spleen). In the lymph nodes and affected internal organs, specific granulomas are formed with central areas of necrosis, accumulation of granulocytes, epithelial and lymphoid elements. The formation of granulomas is facilitated by the incompleteness of phagocytosis, due to the properties of the pathogen (the presence of factors that prevent intracellular killing). The formation of granulomas in primary buboes often leads to their suppuration and spontaneous opening, followed by prolonged healing of the ulcer. Secondary buboes, as a rule, do not suppurate. In the case of replacement of necrotic areas in the lymph nodes with connective tissue, suppuration does not occur, the buboes are absorbed or sclerosed.

Symptoms of Tularemia

In accordance with clinical classification, distinguish the following forms of tularemia:
by localization of the local process: bubonic, ulcerative-bubonic, ocular-bubonic, anginal-bubonic, pulmonary, abdominal, generalized;
according to the duration of the course: acute, protracted, recurrent;
according to severity: mild, moderate, severe.

incubation period. It lasts from 1 to 30 days, most often it is 3-7 days.

Signs of the disease, common to all clinical forms, are expressed in an increase in body temperature up to 38-40 ° C with the development of other symptoms of intoxication - chills, headache, muscle pain, general weakness, anorexia. Fever can be relapsing (most often), constant, intermittent, undulating (in the form of two or three waves). The duration of fever is different, from 1 week to 2-3 months, most often it lasts 2-3 weeks. When examining patients, hyperemia and pastosity of the face, as well as the mucous membrane of the mouth and nasopharynx, injection of the sclera, hyperemia of the conjunctiva are noted. In some cases, an exanthema of a different nature appears: erythematous, maculo-papular, roseolous, vesicular or petechial. The pulse is slowed down (relative bradycardia), blood pressure is reduced. A few days after the onset of the disease, hepatolienal syndrome develops.

The development of various clinical forms of the disease is associated with the mechanism of infection and the entrance gates of infection, which determine the localization of the local process. After the penetration of the pathogen through the skin, a bubonic form develops in the form of regional lymphadenitis (bubo) in relation to the gate of infection. Possible isolated or combined lesion various groups lymph nodes - axillary, inguinal, femoral. In addition, with hematogenous dissemination of pathogens, secondary buboes can form. Soreness occurs, and then an increase in lymph nodes to the size of a hazelnut or a small chicken egg. In this case, pain reactions gradually decrease and disappear. The contours of the bubo remain distinct, the phenomena of periadenitis are insignificant. In the dynamics of the disease, buboes slowly (sometimes over several months) resolve, suppurate with the formation of a fistula and the release of creamy pus, or sclerosis.

Ulcerative bubonic form. More often develops with transmissible infection. At the site of introduction of the microorganism, a spot, papule, vesicle, pustule, and then a shallow ulcer with raised edges successively replace each other for several days. The bottom of the ulcer is covered with a dark crust in the form of a "cockade". At the same time, regional lymphadenitis (bubo) develops. Subsequent scarring of the ulcer occurs slowly.

In cases of penetration of the pathogen through the conjunctiva, an oculo-bubonic form of tularemia occurs. In this case, the mucous membranes of the eyes are affected in the form of conjunctivitis, papular, and then erosive-ulcerative formations with a separation of yellowish pus. Corneal lesions are rare. These clinical manifestations are accompanied by pronounced edema of the eyelids and regional lymphadenitis. The course of the disease is usually quite severe and prolonged.

Anginal-bubonic form. It develops after the pathogen enters with infected food or water. Patients complain of moderate pain in the throat, difficulty swallowing. On examination, the tonsils are hyperemic, enlarged and edematous, soldered to the surrounding tissue. On their surface, more often on one side, grayish-white necrotic deposits are formed, which are difficult to remove. Swelling of the palatine arches and uvula is pronounced. In the future, the tissue of the tonsil is destroyed with the formation of deep, slowly healing ulcers, followed by the formation of a scar. Tularemia buboes occur in the submandibular, cervical and parotid regions, more often on the side of the affected tonsil.

Abdominal shape. It develops as a result of damage to the mesenteric lymph nodes. Clinically manifested by severe abdominal pain, nausea, occasionally vomiting, anorexia. Sometimes diarrhea develops. On palpation, pain is noted near the navel, possible positive symptoms peritoneal irritation. As a rule, hepatolienal syndrome is formed. It is rare to palpate mesenteric lymph nodes, their enlargement is determined by ultrasound.

Pulmonary form. It proceeds in the form of a bronchitis or pneumonic variant.
The bronchitis variant is caused by damage to the bronchial, mediastinal, paratracheal lymph nodes. Against the background of moderate intoxication, a dry cough appears, pain behind the sternum, dry rales are heard in the lungs. Usually this option proceeds easily and ends with recovery in 10-12 days.
The pneumatic version is characterized acute onset, sluggish, debilitating course with high prolonged fever. Pathology in the lungs is clinically manifested by focal pneumonia. Pneumonia is distinguished by a rather severe and acyclic course, a tendency to develop complications (segmental, lobular or disseminated pneumonia, accompanied by an increase in the above groups of lymph nodes, bronchiectasis, abscesses, pleurisy, cavities, lung gangrene).

Generalized form. Clinically resembles typhoid paratyphoid infections or severe sepsis. high fever becomes incorrectly remitting, persists for a long time. Symptoms of intoxication are expressed: headache, chills, myalgia, weakness. Confusion, delusions, hallucinations are possible. The pulse is labile, heart sounds are muffled, blood pressure is low. In most cases, hepatolienal syndrome develops from the first days of the disease. In the future, a persistent exanthema of a roseolous and petechial nature may appear with the localization of rash elements on symmetrical parts of the body - forearms and hands, shins and feet, on the neck and face. With this form, the development of secondary buboes due to hematogenous dissemination of pathogens and metastatic specific pneumonia is possible.

Complications
In most cases, they develop with a generalized form. The most common secondary tularemia pneumonia. Infectious-toxic shock is possible. In rare cases, meningitis and meningoencephalitis, myocarditis, polyarthritis, etc. are observed.

Diagnosis of Tularemia

Tularemia should be distinguished from lymphadenitis of coccal, tuberculous and other etiologies, lymphogranulomatosis, pneumonia (with pulmonary form), lymphosarcoma, felinosis, infectious mononucleosis, ornithosis, Q fever, in natural foci - from the plague.

Tularemia lymphadenitis is distinguished by subsidence of pain with an increase in bubo, weak or absent phenomena of periadenitis, slow resorption or sclerosis, and when suppurating bubo, the creamy nature of pus. Of the signs of the disease, common to all forms of tularemia, pay attention to high prolonged fever, relative bradycardia, hepatolienal syndrome, the possibility of exanthema of a different nature.

In the ulcerative-bubonic form, the development of the primary affect at the site of the introduction of the pathogen is characteristic in the form of spots, papules, vesicles, pustules, and ulcers successively replacing each other. In the oculo-bubonic form of tularemia, the mucous membranes of the eyes are affected in the form of conjunctivitis, papular, and then erosive-ulcerative formations with yellowish pus. Angina in the anginal-bubonic form of the disease is more often distinguished by a one-sided character, moderate sore throat, adhesion of the tonsils to the surrounding fiber, greyish-white plaques that are difficult to remove on their surface, and later the formation of deep ulcers that slowly heal with scarring. Lesions of the mesenteric lymph nodes in the abdominal form are clinically manifested by severe abdominal pain, nausea, occasionally vomiting, and anorexia. The bronchial variant of the pulmonary form of tularemia is distinguished by the defeat of bronchial, mediastinal, paratracheal lymph nodes, tularemia pneumonia - a rather severe acyclic course, a tendency to develop complications (bronchiectasis, abscesses, pleurisy, cavities, lung gangrene).

Laboratory diagnostics
In the first days of the disease in the peripheral blood, moderate leukocytosis, a neutrophilic shift to the left, increase in ESR. In the future, leukocytosis can replace leukopenia with lymphocytosis and monocytosis. IN clinical practice Serological research methods are widely used - RA (minimum diagnostic titer 1:100) and RNHA with an increase in antibody titer in the course of the disease. ELISA on a solid-phase carrier is positive from 6-10 days after the disease, diagnostic titer 1:400; it is 10-20 times more sensitive than other methods serological diagnosis tularemia. It is also common to perform a skin-allergic test with tularin: 0.1 ml of the drug is injected intradermally into the middle third of the forearm with inside; the result of the reaction is taken into account after 1-2 days. The test is highly specific and effective already on early stages(on the 3rd-5th day) of illness. Its positive result is expressed in the appearance of infiltrate, soreness and hyperemia with a diameter of at least 0.5 cm. It should be borne in mind that the test can also be positive in people who have had tularemia.

Bacteriological diagnosis of tularemia is of secondary importance, since the isolation of the pathogen from the blood or other pathological materials is difficult and not always effective. Isolation of the pathogen is possible in the first 7-10 days of the disease, but this requires special media and laboratory animals. Isolation of the pathogen, as well as the production of a biological sample with infection of white mice or guinea pigs bubo punctate, blood of patients, discharge of the conjunctiva and ulcers are possible only in special laboratories especially for working with pathogens dangerous infections. Molecular genetic method: PCR is positive in the initial febrile period of the disease and is a valuable method for the early diagnosis of tularemia.

Treatment of Tularemia

Etiotropic therapy involves the combined use of streptomycin 1 g / day and gentamicin 80 mg 3 times a day intramuscularly. You can prescribe doxycycline 0.2 g / day orally, kanamycin 0.5 g 4 times a day and sisomycin 0.1 g 3 times a day intramuscularly. The course of antibiotic treatment is continued until the 5-7th day. normal temperature body. The second line of antibiotics includes cephalosporins III generation, rifampicin and chloramphenicol.

Detoxification therapy is carried out, antihistamines and anti-inflammatory drugs (salicylates), vitamins, cardiovascular agents are indicated. For local treatment buboes and skin ulcers, ointment dressings, compresses, laser irradiation, diathermy are used. In case of suppuration of the bubo, it is opened and drained.

Patients are discharged from the hospital after clinical recovery. Long-term non-absorbable and sclerosed buboes are not a contraindication for discharge.

Prevention of Tularemia

Epizootologo-epidemiological surveillance
It includes constant monitoring of the incidence of people and animals in natural foci of tularemia, the circulation of the pathogen among animals and blood-sucking arthropods, monitoring the state of immunity in humans. Its results form the basis for planning and implementing a set of preventive and anti-epidemic measures. Epidemiological surveillance provides for epizootological and epidemiological examination of natural foci of tularemia, generalization and analysis of the data obtained in this case, causing epidemic manifestations in natural foci of tularemia in the form of sporadic, group and outbreaks of human morbidity.

Preventive actions
The basis for the prevention of tularemia is made up of measures to neutralize the sources of the infectious agent, neutralize the transmission factors and vectors of the pathogen, as well as the vaccination of threatened contingents of the population. Elimination of the conditions of infection of people (general sanitary and hygienic measures, including sanitary and educational work) has its own characteristics when various types morbidity. In case of transmissible infections through bloodsucking, repellents, protective clothing are used, and the access of the unvaccinated population to unfavorable territories is restricted. Of great importance is the fight against rodents and arthropods (deratization and pest control measures). For the prevention of alimentary infection, bathing in open water should be avoided, and for household and drinking purposes, only boiled water. When hunting, it is necessary to disinfect hands after skinning and gutting hares, muskrats, moles and water rats. Vaccination is carried out in a planned manner (among the population living in natural foci of tularemia and contingents at risk of infection) and according to epidemiological indications (unscheduled) when the epidemiological and epizootological situation worsens and there is a threat of infection of certain population groups. For immunoprophylaxis, a live attenuated vaccine is used. Vaccination ensures the formation of stable and long-term immunity in vaccinated (5-7 years or more). Revaccination is carried out after 5 years for contingents subject to routine vaccination.

Activities in the epidemic focus
Each case of human disease with tularemia requires a detailed epidemiological and epidemiological examination of the focus with clarification of the route of infection. The question of hospitalization of a patient with tularemia, the timing of discharge from the hospital is decided by the attending physician purely individually. Patients with abdominal, pulmonary, ocular-bubonic and anginal-bubonic, as well as moderate or severe cases of ulcerative-bubonic and bubonic forms must be hospitalized according to clinical indications. Patients are discharged from the hospital after clinical recovery. Long-term non-absorbable and sclerosed buboes are not a contraindication for discharge. Dispensary observation for those who have been ill, they are carried out for 6-12 months in the presence of residual effects. Separation of other persons in the outbreak is not carried out. As a measure of emergency prevention, antibiotic prophylaxis can be carried out by prescribing rifampicin 0.3 g 2 times a day, doxycycline 0.2 g 1 time a day, tetracycline 0.5 g 3 times a day. The patient's home is disinfected. Only things contaminated with secretions of patients are subject to disinfection.