Tularemia signs of the disease. Diagnosis and treatment of tularemia. General characteristics of the disease

Tularemia is an infectious disease that is characterized by natural focality, causes inflammation 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 environmental objects. 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, which is not difficult to diagnose, responds well 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 pain in the abdomen, nausea, vomiting, open intestinal bleeding (not all patients appear). 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 for a person and can go away on its own, but specific treatment can speed up this process, saves a person from contemplating ugly sores. The pulmonary form causes much more dramatic consequences and requires an 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 refers to an acute natural focal infection that mainly affects the lymphatic system and skin. In some cases, the respiratory organs, the mucous membrane of the throat and eyes suffer. The course of the disease is accompanied by prolonged fever, general intoxication of the body, lymphadenitis, rash, hepatosplenomegaly (simultaneous enlargement of the spleen and liver) and other signs.

Tularemia is an acute infection of bacterial etiology, which is manifested by severe fever, lymphadenitis and skin manifestations at the sites of infection.

Forms of tularemia

Tularemia is diagnosed during a skin-allergic test, polymerase chain reaction, various serological reactions. Treatment is divided into conservative, which includes a set of measures to combat intoxication and antibacterial therapy, and surgical, which comes down to opening bubonic nodes and installing drains.

The types of this disease are classified as follows:

  1. According to the method of infection, they are divided into pulmonary, ulcerative-bubonic, generalized, anginal-bubonic, bubonic, abdominal, oculobubonic forms.
  2. The severity of the disease: severe, moderate, mild.
  3. According to the duration of the course: protracted, acute, recurrent.

Natural foci of tularemia are located mainly in the northern hemisphere, on the territory of the Russian Federation, the bulk of the foci is located in Western Siberia and the European part of Russia. Tularemia is included in the list of especially dangerous infections by epidemiologists.

Note!Tularemia is causedFrancisellatularensis is an aerobic Gram-negative rod bacterium. This pathogen has an enviable vitality. The death of the tularemia bacillus occurs when exposed to disinfectants and high temperature.

Natural source of infection are wild animals and birds. Most often, rodents are infected (muskrats, voles, chipmunks, and others), but larger animals (sheep, dogs, foxes, hares, and others) can also become infected. From a sick person, the pathogen is not transmitted. With the transmissible mechanism of transmission of the pathogen, animals become infected with other bloodsuckers.

Humans become infected through direct contact with sick animals, such as during skinning or carcass cutting, or through consumption of food and water contaminated with tularemia bacilli.

The infection can also enter the human body through the respiratory route - to put it simply, at various agricultural productions, a person can inhale dust contaminated with bacteria. When the causative agent of tularemia enters the human body, the development of the disease is inevitable.

Symptoms of tularemia in humans

Tularemia has a rather vague incubation period, lasting from one day to one month, but, as a rule, symptoms appear within the first week. Initially, there is a sharp increase in body temperature, up to forty degrees. Against the background of elevated temperature, symptoms of intoxication of the body increase in the form of severe and muscle pain, general weakness. The fever can keep both constantly and proceed in the form of two or three waves. The patient's fever is usually up to three weeks, but in some cases this condition can last up to three months.

During the initial examination of the patient, redness of the face, eye sclera, mucous membranes of the nasopharynx and oral cavity is observed. There may be a slight swelling of the skin and an injection of the sclera, in which the eyes turn red. Arterial, slow heartbeat. A few days after the onset of fever, an enlargement of the liver and spleen is observed at the same time, and a rash of a different nature may appear on the skin.

Depending on the method of infection, the clinical picture of the disease also differs:

The most severe form of tularemia is the generalized form. Its course is very similar to sepsis, or typhoid and paratyphoid infections. There is a pronounced intoxication, prolonged, incorrectly remitting, fever, severe muscle and headaches, confusion, hallucinations, delirium.

Complications occur, as a rule, with a generalized form of tularemia. The most common complication is secondary pneumonia. Possible occurrence, meningoencephalitis, pericarditis, and even infectious-toxic shock.

Diagnostic measures

Diagnosis of tularemia is possible only with the help of laboratory tests.

Non-specific laboratory methods are general urinalysis and. These studies will directly indicate the presence of inflammation and intoxication in the body. At the initial stage of the disease, a general blood test will show neutrophilic leukocytosis, over time, the number of leukocytes decreases, and the concentration of monocytes and lymphocytes increases.

Specific serological diagnosis is carried out using the indirect hemagglutination reaction and the direct agglutination reaction. In the process of development of the pathological process, an increase in the titer of specific antibodies is recorded. A week after the onset of the disease, an immunofluorescence assay, which is the most sensitive serological test for tularemia, should be performed. For early diagnosis, it is used, which allows you to identify pathology literally in the first days. An allergic skin test with tularemic toxin shows the disease in the first week.

Important! Bacteriological culture is practically not used to identify the causative agent of tularemia, since it is rather difficult to isolate bacteria from biomaterials and blood.

To confirm the pulmonary form of the disease, the lungs are used; in the absence of a tomograph, it is possible to carry out.

Treatment of tularemia

In view of the fact that tularemia belongs to the category of especially dangerous diseases, its treatment is carried out in an infectious diseases hospital.. To destroy the pathogen in the body, a wide spectrum of action is prescribed (gentomycin, kanamycin, doxycycline). In case of ineffectiveness of the prescribed treatment, second-line antibiotics (rifampicin, levomycetin, third-generation cephalosporins) are prescribed.

With severe intoxication, infusion detoxification therapy is performed. Antipyretic, anti-inflammatory drugs, vitamins are prescribed. Open sores on the skin are covered with bandages. Buboes that have undergone suppuration are opened by surgical methods, followed by drainage.

Prevention

Important! The main method of prevention is the vaccination of people with tularemia vaccine in epidemically disadvantaged areas. Strong immunity lasts up to seven years, so re-vaccination is carried out after five years. If there is a threat of an epidemic, emergency prophylaxis is possible by administering antibiotics intravenously.

Anti-epidemic measures include the suppression of possible routes of transmission of the tularemia pathogen and disinfection of sources of infection. In epidemically disadvantaged areas, at agricultural enterprises and catering facilities, a full range of measures is being taken to combat the spread of infection (disinfection, disinfestation, deratization).

It is necessary to pay special attention to individual protection against the causative agent of tularemia for people involved in hunting wild animals, especially in the process of skinning and butchering carcasses and for persons taking part in deratization activities when collecting rodent carcasses. Hands must be protected with rubber gloves, after removing which it is imperative to disinfect the skin. Water is allowed to be consumed only from reliable proven sources.

If a person with tularemia is identified, then all things that could have been infected must be disinfected.

Tularemia (lat. tularemia; plague-like disease, rabbit fever, small plague, mouse disease, deer fly fever, epidemic lymphadenitis) is an acute zoonotic bacterial natural focal infectious disease with a variety of pathogen transmission mechanisms. It is characterized by fever, intoxication, inflammatory changes in the area of ​​the entrance gate of infection, regional lymphadenitis.

ICD-10 codes

A21.0. Ulceroglandular tularemia.
A21.1. Oculoglandular tularemia.
A21.2. Pulmonary tularemia.
A21.3. Gastrointestinal tularemia.
A21.8. Other forms of tularemia.
A21.9. Tularemia, unspecified.

Etiology (causes) of tularemia

Pathogen - Francisella tularensis, genus Francisella, family Brucellaceae. Gram-negative polymorphic (mainly coccoid) immobile rod that does not form spores and capsules. Facultative anaerobe. The pathogen is demanding on cultivation conditions, grows on nutrient media with the addition of cysteine ​​or egg yolk, defibrinated rabbit blood, tissue extracts (liver, spleen, brain) and other growth stimulants. Of laboratory animals, white mice and guinea pigs have an increased susceptibility to tularemia.

The microorganism contains somatic (O) and shell (Vi) antigens, which are associated with the virulence and immunogenic properties of the pathogen. The main pathogenicity factor is endotoxin.

F. tularensis is stable in the environment, especially at low temperatures and high humidity (survives at –300°C, persists in ice for up to 10 months, and in frozen meat for up to 3 months). The causative agent is less resistant to drying (in the skins of rodents that have died from tularemia, it persists for up to 1.5 months, at a temperature of 30 ° C - up to 1 week); remains viable in river water at a temperature of 10 ° C for up to 9 months, in soil - up to 2.5 months, in milk - up to 8 days, on grain and straw at -5 ° C - up to 192 days, at a temperature of 20–30 ° C - up to 3 weeks. At the same time, F. tularensis is very sensitive to insolation, ultraviolet irradiation, ionizing radiation, high temperature, and disinfectants (sublimes die in 3–5 min under the action of solutions of lysol, chloramine, and bleach).

For complete disinfection, the corpses of infected animals are kept in a disinfectant solution for at least a day, after which they are burned.

The pathogen is sensitive to chloramphenicol, rifampicin, streptomycin and other aminoglycosides, antibiotics of the tetracycline group.

Epidemiology of tularemia

Tularemia is a classic natural focal disease, an obligate zoonosis. About 150 species of animals, including 105 species of mammals, 25 species of birds, several species of fish, frogs, and other aquatic organisms serve as the source of the infectious agent. On the territory of Russia, the main reservoir and source of infection are rodents (mouse, rabbits, hares, water rats, muskrats, hamsters, etc.). Excretions and corpses of dead animals contain a large number of pathogens that inseminate environmental objects, including water, and remain in them for a long time. Between rodents, the transmission of infection is carried out by the alimentary route. Among domestic animals, the reservoir of infection can be sheep, pigs, cattle, horses, but infection of people most often occurs in natural foci through direct and indirect contact with rodents. A sick person cannot be a source of infection for others.

Infection carriers that support the existence of the pathogen in natural foci are blood-sucking insects (ixodid and gamasid mites, mosquitoes, horseflies).

The pathogen can enter the human body through microtraumas of the skin and intact mucous membrane of the tonsils, oropharynx, gastrointestinal tract, respiratory tract, eyes.

There are four mechanisms of transmission of the pathogen:

  • contact - in contact with infected rodents (cutting carcasses, skinning) and water (bathing, washing, rinsing clothes);
  • alimentary - when using infected, thermally untreated foods and water;
  • aerosol - by inhalation of infected dust through the mouth and nose during winnowing and threshing grain, stacking hay and straw;
  • transmissive (main) - when bitten by infected blood-sucking insects or crushed.

The pulmonary form of tularemia occurs with aerosol infection, anginal-bubonic and abdominal - with alimentary, ulcerative-bubonic and oculobubonic - with transmissible and contact infection.

The susceptibility of people to tularemia is high (reaches 100%). Celebrate the summer-autumn seasonality. Human infection occurs mainly in rural areas, but in recent years, urban residents predominate among the sick (up to 2/3), which is associated with the desire of citizens to relax in nature, as well as with the use of thermally untreated agricultural products.

Persons who have had the disease acquire stable, long-lasting, but not absolute immunity.

Natural foci of tularemia exist on all continents of the Northern Hemisphere, in the countries of Western and Eastern Europe, in Asia, and North America. On the territory of the Russian Federation, the disease is registered in almost all regions, regions, autonomous republics, while 75% of cases are in the Northern, Central and West Siberian regions of Russia. Recently, the incidence of tularemia ranges from fifty to several hundred people a year. An increase in the number of cases is noted in years of increased numbers of rodents.

Tularemia pathogenesis

F. tularensis enters the human body through the skin (even externally intact) and mucous membranes of the eyes, respiratory tract, tonsils, and gastrointestinal tract. When infected through the skin or by aerogenic means, fifty viable microorganisms are sufficient for the development of the disease, and with alimentary infection, more than 108 microbial cells.

At the site of the entrance gate of infection, the pathogen multiplies with the development of a necrotic-inflammatory reaction and primary affect (skin ulcer, passing through the stages of papules, vesicles and pustules; on the tonsils - necrotic tonsillitis, in the lungs - focal necrotic pneumonia, on the conjunctiva - conjunctivitis). Then the pathogen penetrates into the regional lymph nodes, causing the development of specific lymphadenitis - the primary bubo. Here, a partial death of bacteria occurs, accompanied by the release of endotoxin (LPS-complex), which enhances the local inflammatory process and causes the development of intoxication when it enters the bloodstream.

In some cases, the pathogen overcomes the lymphatic barrier and spreads hematogenously (generalization of the process), causing damage to other groups of lymph nodes that are not associated with the place of introduction of the microorganism (secondary buboes) and internal organs (liver, spleen, lungs). The death of the pathogen circulating in the blood and the release of endotoxin aggravate intoxication. A significant role in the pathogenesis of the disease is played by specific sensitization and allergization of the body.

Relapses are possible associated with long-term intracellular persistence of the pathogen in a latent state in specific foci and macrophages, with incomplete phagocytosis, the formation of a protein by F. tularensis, which contributes to the suppression of TNF-α and IL-1 and the long-term preservation of the microorganism.

Tularemia is characterized by a granulomatous type of inflammation as a result of incomplete phagocytosis. Granulomas are formed in the lymph nodes and internal organs (usually in the liver and spleen) from epithelial cells, polymorphonuclear leukocytes and lymphocytes. In appearance and cellular composition, tularemia granulomas resemble those of tuberculosis. They are subject to necrosis and suppuration, followed by replacement with connective tissue. In places of accumulation of granulomas, the formation of abscesses is possible. In acute forms of tularemia, necrotic changes predominate, in subacute forms, signs of reactive inflammation.

The granulomatous process is most pronounced in the regional lymph nodes, where primary lymphadenitis (bubo) develops. With its suppuration and opening, a long-term non-healing ulcer forms on the skin. Suppuration usually does not occur in secondary buboes.

With aerosol infection, the most pronounced changes in the form of foci of alveolar necrosis, infiltration and granuloma formation are observed in the tracheobronchial lymph nodes and lung parenchyma. In the heart and kidneys, dystrophic changes are noted, in the intestines - lesions of Peyer's patches and mesenteric lymph nodes.

Clinical picture (symptoms) of tularemia

Incubation period ranges from several hours to 3 weeks (average 3-7 days).

In accordance with the classification of G.P. Rudneva (1960) distinguish several forms of the disease (Table 17-27).

Tab. 17-27. Forms of tularemia and the mechanism of infection

* In parentheses are the names corresponding to the International Statistical Classification of Diseases (Tenth Revision) WHO (1995).

According to the severity of the infectious process, mild, moderate and severe forms of tularemia are distinguished.

According to the duration of the course, acute (up to 3 months), protracted (up to 6 months), recurrent forms of tularemia and, in addition, inapparent (asymptomatic, latent) tularemia are distinguished, which is detected mainly during epidemic outbreaks in a laboratory study.

Tularemia proceeds cyclically. The following periods of the disease are distinguished: incubation, initial, peak period and recovery.

Symptoms of the initial period are the same in all clinical forms. Typically acute onset with chills, fever, and symptoms of intoxication. The temperature rises to 38–40 °С and higher within a few hours. At the same time, headache, dizziness, weakness, fatigue, muscle pain (especially in the lumbar region and calf muscles), loss of appetite, sleep disturbances, and excessive sweating occur. Bradycardia, hypotension, hepatosplenomegaly are possible.

The duration of the initial period is 2–3 days. Later, there are signs characteristic of one or another clinical form, but the common symptoms for all forms are fever, the characteristic appearance of the patient and intoxication.

The duration of the febrile period is 2–3 weeks (from 5–7 to 30 days), but sometimes, with a recurrent course or complications, it can be extended up to several months. The nature of the temperature curve can be different: remitting (mainly), incorrectly intermittent, constant, undulating. The period of convalescence may be accompanied by prolonged subfebrile condition.

The appearance of patients is characteristic: the face is puffy and hyperemic, in severe cases it is bluish-purple in color (especially around the eyes, lips, earlobes). Often, a pale triangle is noted around the chin, signs of conjunctivitis, injection of scleral vessels, petechial hemorrhages on the oral mucosa are found. Nosebleeds are possible. Patients are euphoric.

On the skin from the third day of illness, an erythematous, papular or petechial rash may occur, which is resolved by lamellar and (or) scaly peeling, pigmentation. Elderly people have erythema nodosum.

The most characteristic signs are considered lymphadenitis of various localization, observed in all forms of the disease.

Bubonic (glandular) form occurs as a result of contact or transmissible infection. The bubo is usually localized in the region of the inguinal, femoral, elbow and axillary lymph nodes. Lymphadenitis is detected 2-3 days after the onset of the disease. Gradually increasing, the lymph nodes reach their maximum size by the 5-8th day of illness. With the involvement of a group of regional lymph nodes in the process, the formation of a conglomerate with signs of periadenitis is possible. The size of the bubo can vary from the size of a hazelnut to 10 cm. The color of the skin above the bubo is not changed at first; mobility is limited, pain is mild. The evolution of the bubo is different. Most often, complete resorption (from the end of the 2nd week) or sclerosis occurs. Less often, suppuration is noted (from the end of the second to the beginning of the third week) and spontaneous opening of the bubo, followed by scarring. At the same time, the skin above it turns red, the lymph node becomes soldered to the skin and becomes more painful, fluctuation occurs. In the future, a fistula is formed, through which thick creamy pus is released. In this case, the healing or resorption of the bubo occurs very slowly, in waves, often with scarring and sclerosis of the lymph node. In this regard, with suppuration and a clear fluctuation, it is recommended to open the knot: this accelerates healing.

There are primary (due to lymphogenous spread of the pathogen) and secondary (due to hematogenous spread of the pathogen) buboes. Secondary buboes are not connected with the entrance gate, they are smaller than the primary ones, do not suppurate and completely resolve.

The outcome and duration of the bubonic form of tularemia depend on the timeliness of specific therapy. Without proper treatment, the duration of the disease can be 3–4 months or more.

At ulcerative bubonic(ulceroglandular) form of tularemia, in contrast to bubonic, at the site of the introduction of the pathogen, a primary affect is formed. It usually develops with transmissible, less often with contact infection. The local process goes through the stages of spots, papules, vesicles and pustules, which, opening up, transforms into a painless small (5–7 mm) ulcer. Its edges are raised, the discharge is serous-purulent, scanty. In 15% of cases, the ulcer goes unnoticed. The usual localization of the primary affect is open parts of the body (neck, forearms, shins).

The local skin process is accompanied by an increase, soreness of the regional lymph nodes and the formation of a bubo with all the characteristic signs. Lymphangitis for the ulcerative-bubonic form of tularemia is not typical. The ulcer heals under the crust rather slowly - within 2-3 weeks or longer. After rejection of the crust, a depigmented spot or scar remains.

Anginal-bubonic (anginal-glandular) form tularemia occurs when contaminated with food or water, in particular when eating insufficiently thermally processed meat (usually hare). In this case, the primary affect is located on the tonsils (more often - on one of them) or on the mucous membrane of the posterior wall of the pharynx, palate. Specific angina is characterized by hyperemia with a bluish tinge and swelling of the tonsils, a grayish-white island or membranous coating. The plaques are removed with difficulty and resemble diphtheria, but they do not spread beyond the tonsils. Under the plaque, after a few days, one or more slowly healing, often scarring ulcers appear. In some cases, the pathological process on the mucous membrane of the pharynx is limited to the symptoms of catarrhal angina. Often there are petechiae. Simultaneously with the development of angina, cervical (usually submandibular) lymphadenitis is observed with all the signs of a tularemia bubo (sizes from a walnut to a chicken egg). Sometimes the formation of a bubo does not coincide in time with the development of the process on the tonsils, lymphadenitis is formed later. With massive infection, a combination of anginal-bubonic and abdominal forms of tularemia is possible, especially in people with low acidity of gastric juice. The disease proceeds with high temperature and intoxication.

The duration of tularemia angina is from 8 to 24 days. In severe cases, specific antibodies are detected late, making it difficult to diagnose the disease.

Abdominal (gastrointestinal) form, as well as anginal-bubonic, occurs with alimentary infection. This is one of the rare but very severe forms of the disease. It is characterized by high fever and severe intoxication. There are intense aching or cramping, diffuse or localized in a certain area of ​​abdominal pain, often imitating a picture of an acute abdomen. The tongue is coated with a gray-white coating, dryish. Nausea, vomiting, flatulence, enlargement of the liver and spleen are possible. From the very beginning of the disease, stool retention or loose stools without pathological impurities are observed.

Cases of ulcerative lesions of the mucous membrane of the ileum and small intestine, the pyloric part of the stomach and duodenum are described. Sometimes it is possible to palpate enlarged and dense mesenteric lymph nodes or their conglomerates. Lymphadenitis may be accompanied by symptoms of peritoneal irritation, and with suppuration and opening of the lymph nodes, peritonitis and intestinal bleeding may develop.

Oculobubonic (oculoglandular, ophthalmic) form tularemia occurs when infected through the conjunctiva, when the pathogen enters the eye through contaminated hands, by airborne dust, when washing with water from infected sources or when bathing. The ophthalmic form of tularemia is quite difficult, but it is observed relatively rarely (1–2% of cases).

Characterized by the development of acute specific, often unilateral conjunctivitis with severe lacrimation and eyelid edema, marked swelling of the transitional folds of the conjunctiva, mucopurulent discharge. On the mucous membrane of the lower eyelid, yellowish-white nodules the size of millet grains, ulcers are noted. Vision is not affected. The process is accompanied by an increase and slight soreness of the parotid, anterior cervical and submandibular lymph nodes. The duration of the disease is from 3 weeks to 3 months or longer. It is possible to develop complications such as dacryocystitis (inflammation of the lacrimal sac), phlegmon, keratitis, corneal perforation.

Pulmonary (thoracic) form with a primary inflammatory process in the lungs are recorded in 11-30% of cases of tularemia. Infection occurs by airborne dust (by inhalation of infected dust during agricultural work).

There are two variants of the pulmonary form - bronchitis and pneumonic.

The bronchial variant, in which the lymph nodes are affected, proceeds relatively easily, with subfebrile body temperature, dry cough, chest pain (with the development of tracheitis). Harsh breathing, scattered dry rales are heard. X-ray examination reveals an increase in tracheobronchial lymph nodes. Clinical recovery occurs in 10-14 days.

The pneumonic variant is more severe and longer (up to 2 months or more), with a tendency to recurrence and abscess formation. A clinical picture of pneumonia (focal, segmental, lobar or disseminated) is detected, which does not have any pathognomonic signs.

Physical data are scarce (dullness of percussion sound, various dry and wet rales) and occur late. Possible involvement in the pathological process of the pleura. Hepato- and splenomegaly are often found.

Radiologically, an increase in the pulmonary pattern (perivascular and peribronchial infiltrates), an increase in hilar, paratracheal and mediastinal lymph nodes, and pleural effusion are determined. All these signs can be detected no earlier than the 7th day of illness. As a result of necrosis of the affected areas of the lung, cavities of various sizes (tularemia cavities) can form.

From the primary pulmonary form of tularemia, it is necessary to distinguish the secondary one, which develops metastatically and can join any form of the disease at a later date.

The pulmonary form of tularemia with timely and proper treatment ends in recovery; mortality does not exceed tenths of a percent (in the past - up to 5%), but is characterized by a long (up to 2 months) course, the development of abscesses, bronchiectasis.

Relapses, as well as a protracted course, often occur with late or inadequate antibiotic therapy. Their development is due to the long-term persistence of the pathogen. There are early (after 3-5 weeks) and late (after several months and even years) relapses. Bubonic tularemia recurs more often: lymphadenitis, localized near the primary bubo or not far from it, minor intoxication, weakness, sweating, sleep disturbance. No fever; sometimes note subfebrile condition. The size of the affected lymph node is usually smaller than in the primary disease; suppuration occurs much less frequently.

Complications are more often noted in the generalized form of tularemia. It is possible to develop ITSH, meningitis, meningoencephalitis, pericarditis, myocardial dystrophy, polyarthritis, vegetative neuroses, peritonitis (due to suppuration and spontaneous opening of mesenteric lymph nodes in the abdominal form), corneal perforation, bronchiectasis, abscess and gangrene of the lungs (with pneumonic form). The course of any form can be complicated by tularemia pneumonia.

Diagnosis of tularemia

Diagnosis of tularemia is based on clinical, epidemiological and laboratory data.

In the general blood test in the initial period, normocytosis or slight leukocytosis, an increase in ESR are detected. The peak period of the disease is characterized by leukopenia with lympho- or monocytosis. Neutrophilic leukocytosis is noted only with suppuration of buboes.

For the specific diagnosis of tularemia, serological and allergic tests, bacteriological examination and a biological sample are used. The main serological methods are RA and RPHA with a diagnostic titer of 1:100 and above (diagnostic standard). The diagnostic value of RPHA is higher, since antibodies in a titer of 1:100 are detected early, by the end of the first week (in RA - from the 10th–15th day). To diagnose an acute disease and determine post-vaccination titers, the study is carried out in dynamics in a week. If antibodies are not detected during the second examination or their titer is not changed, then the patient's blood is examined a week after the second examination for the third time (order of the Ministry of Health of the Russian Federation No. 125 of 04/14/99). An increase in antibody titer by 2–4 times in RA and RPHA confirms the diagnosis of tularemia. Lack of growth indicates the anamnestic nature of the reaction. Other serological methods for diagnosing tularemia have also been developed: RPHA, ELISA. ELISA on a solid-phase carrier is positive from the 6th–10th day of the disease (diagnostic titer 1:400); in terms of sensitivity, it is 10–20 times higher than other methods of serodiagnosis.

In the diagnosis of tularemia can be used (in accordance with the appendix to the order of the Committee of Health and the Center for State Sanitary and Epidemiological Surveillance of Moscow No. 437/47 dated September 28, 1999) an allergic skin test, which is distinguished by strict specificity. It is classified as an early diagnostic method, since it becomes positive already from the 3-5th day of illness. Tularin is administered intradermally or cutaneously (in strict accordance with the applicable instructions) in the middle third of the palmar surface of the forearm. The result is taken into account after 24, 48 and 72 hours. The sample is considered positive if the diameter of the infiltrate and hyperemia is not less than 0.5 cm. Only one hyperemia disappearing after 24 hours is regarded as a negative result. The test with tularin does not allow distinguishing recent cases of the disease from anamnestic and vaccination reactions. When there are contraindications to the use of a skin test (increased sensitization), they resort to the method of in vitro allergy diagnostics - the leukocytolysis reaction.

An auxiliary role is played by bacteriological methods and a biological test, which can only be carried out in specially equipped laboratories that have permission to work with the causative agent of tularemia. PCR, which can detect specific DNA in various biological substrates, is positive in the initial febrile period of the disease, so it is considered a valuable method for the early diagnosis of tularemia.

Differential Diagnosis

When conducting differential diagnosis in the initial period of the disease, it is necessary to exclude influenza, typhoid and typhus, pneumonia, and subsequently - plague, anthrax, ulcerative necrotic tonsillitis, diphtheria, nonspecific lymphadenitis, tuberculosis, sepsis, malaria, brucellosis, mumps, benign lymphoreticulosis , Infectious mononucleosis.

Plague is characterized by more pronounced intoxication. Plague bubo is characterized by severe pain, density, blurring of contours, periadenitis, skin hyperemia, and an increase in local temperature. The plague bubo rarely resolves, but suppurates and opens earlier than with tularemia (after 1 and 3 weeks, respectively). The predominant localization of the bubo in plague is the region of the inguinal and femoral lymph nodes (with tularemia, they are less often affected). An ulcer in tularemia is less painful than in plague, or generally painless. With plague, severe complications and an unfavorable outcome are more likely to occur.

Tularemia pneumonia differs from plague pneumonia in the absence of bloody sputum (with rare exceptions). Patients with tularemia are not contagious. It should be taken into account that the distribution areas of plague and tularemia do not coincide.

Nonspecific lymphadenitis (staphylococcal and streptococcal) is often accompanied by lymphangitis and periadenitis. They are characterized by severe soreness and hyperemia of the skin, early suppuration (compared to tularemia). Their occurrence is usually preceded by a primary purulent focus in the form of panaritium, furuncle, carbuncle, infected wound, abrasion, etc. Fever and symptoms of intoxication are often absent or occur later than lymphadenitis. In the hemogram, unlike tularemia, neutrophilic leukocytosis and an increase in ESR are recorded.

The anginal-bubonic form of tularemia is differentiated from the usual sore throat. Tularemia is characterized by unilateral tonsillitis; plaques on the tonsils resemble those of diphtheria; after their rejection, an ulcer is found. Regional (submandibular) lymph nodes are enlarged significantly, but they are practically painless on palpation. Sore throat is less intense than with tonsillitis, and occurs later (after 2-3 days).

Unlike diphtheria, angina with tularemia is characterized by a more acute onset, usually one-sided localization and rarely spreading beyond the tonsils. The results of laboratory tests are of decisive importance.

With tuberculous lymphadenitis, the disease begins gradually, with subfebrile temperature. Lymph nodes are dense, painless, smaller than in tularemia.

Ulcers on the skin with tularemia differ from anthrax in soreness, smaller size, absence of a black scab and swelling of the surrounding tissues.

Tularemia pneumonia differs from lobar pneumonia in a less violent onset, more moderate toxicosis and a sluggish course.

For benign lymphoreticulosis (felinosis), as well as for tularemia, the presence of a primary affect in the area of ​​​​the gate of infection and bubo (more often in the area of ​​\u200b\u200bthe axillary and ulnar lymph nodes) is characteristic. The most important indication of contact with a cat (90-95% of patients) in the form of a scratch or bite. The course of the disease is benign, intoxication is not expressed.

Indications for consulting other specialists

With suppuration of the bubo - consult a surgeon, with a pneumonic form - a phthisiatrician, with an oculo-glandular form - an ophthalmologist.

Diagnosis example

A21.0. Ulceroglandular tularemia of moderate severity, acute course of the disease.

Treatment of tularemia

Patients with suspected tularemia are hospitalized according to clinical indications. Windows in rooms should be covered with mesh to prevent the transmission of infection.

In the acute period, patients need bed rest and good nutrition enriched with vitamins. Care is of great importance. Medical personnel should monitor compliance with sanitary and hygienic rules and conduct ongoing disinfection using a 5% phenol solution, a sublimate solution (1: 1000) and other disinfectants.

The main etiotropic drugs are aminoglycosides and tetracyclines (standard of care).

Streptomycin is prescribed 0.5 g twice a day intramuscularly, and with a pulmonary or generalized form - 1 g twice a day. Gentamicin is used parenterally at 3-5 mg / kg per day in 1-2 doses; amikacin - 10-15 mg / kg per day in 2-3 doses.

With timely treatment of bubonic and ulcerative-bubonic forms of moderate tularemia, it is possible to ingest doxycycline at a daily dose of 0.2 g or tetracycline 0.5 g four times a day. Tetracyclines are not prescribed for pregnant women, children under eight years of age, people with impaired renal function, liver, severe lymphopenia.

The second row of antibiotics includes third-generation cephalosporins, rifampicin, chloramphenicol, fluoroquinolones, used in age doses. Currently, in the treatment of tularemia, ciprofloxacin is considered as an alternative drug to aminoglycosides.

The duration of the course of antibiotic therapy is 10–14 days (up to the 5–7th day of normal temperature). In case of relapse, an antibiotic is prescribed, which was not used during the first wave of the disease, while simultaneously lengthening the course of antibiotic therapy.

In the presence of skin ulcers and buboes (before the onset of suppuration), local compresses, ointment dressings, thermal procedures, heating with sollux, blue light, quartz, laser irradiation, and diathermy are recommended.

In case of suppuration of the bubo, the occurrence of fluctuation, surgical intervention is necessary: ​​opening the lymph node with a wide incision, emptying it from pus and necrotic masses and draining it. Do not open a vesicle or pustule at the site of an insect bite.

Pathogenetic therapy, including detoxification, antihistamines and anti-inflammatory drugs (salicylates), vitamins and cardiovascular agents, is carried out according to indications. If the eyes are affected (oculobubonic form), they must be washed 2-3 times a day and instilled with a 20-30% solution of sodium sulfacyl; with angina, rinsing with nitrofural, a weak solution of potassium permanganate, is prescribed.

The patient can be discharged from the hospital within a week at normal temperature, satisfactory condition, scarring of skin ulcers, reduction of mobile and painless lymph nodes to the size of a bean or plum stone. Bubo sclerosis is not considered a contraindication to discharge. Patients who have undergone an abdominal form are discharged at a stable normal temperature for a week or more, with normal gastrointestinal function. The discharge of patients who have recovered from the oculoglandular form is carried out after consulting an ophthalmologist. When a patient is discharged after a pulmonary form of tularemia, it is necessary to conduct a control fluoroscopy or chest x-ray.

Tularemia prognosis

The prognosis for common forms of the disease is favorable, for pulmonary and generalized forms it is serious. Mortality does not exceed 0.5–1% (according to American authors, 5–10%).

During the period of convalescence, prolonged low-grade fever, asthenic syndrome are typical, residual phenomena (enlarged lymph nodes, changes in the lungs) may persist. In a number of patients, the ability to work is restored slowly, which requires a medical-labor examination.

Clinical examination

There is no consensus regarding the conduct of dispensary observation. In the current order of the Ministry of Health of the Russian Federation No. 125 dated April 14, 1999, the need for medical examination is not specified, but due to the possibility of late relapses, a number of authors recommend establishing dispensary observation of those who have been ill for 1.5–2 years.

Measures to prevent tularemia

Specific prophylaxis

The basis of specific prophylaxis is the vaccination of persons older than seven years old, staying or working in a territory endemic for tularemia. Apply a live dry tularemia vaccine developed by B.Ya. Elbert and N.A. Gaisky. On the 5–7th and 12–15th day, the intensity of immunity is assessed. If the result is negative, re-vaccination is carried out. The state of immunity in vaccinated people is checked five years after vaccination and subsequently once every two years. Revaccination is carried out with negative results of immunological (allergic or serological) reactions. The need for vaccination is determined by the territorial centers of the State Sanitary and Epidemiological Supervision on the basis of an analysis of the epidemiological situation in the territory under their jurisdiction. There are scheduled and unscheduled (according to epidemic indications) vaccination.

The state of immunity in the population is determined by random testing of the adult working population using allergic or serological methods: RA, RPHA, ELISA. Revaccination is carried out at a level of IIP below 70% in meadow-field foci and less than 90% in floodplain and marsh foci, as well as according to epidemic indications.

Non-specific prophylaxis provides for control over natural foci of tularemia, timely detection of epizootics among wild animals, carrying out deratization and pest control measures.

In case of a water outbreak, it is forbidden to use unboiled water and bathe, and in case of contamination of well water, measures are taken to clean the well from the corpses of rodents and disinfect the water.

To prevent commercial infections, it is advisable to use gloves when removing skins from dead rodents and disinfect hands. Carry out measures for disinfestation and disinfection in warehouses for storing skins. Careful heat treatment of meat (for example, hare) is necessary before eating.

When stacking hay and threshing bread, they use canned glasses and protective masks.

Among the population of areas unfavorable for tularemia, it is necessary to carry out systematic explanatory and sanitary-educational work.

Persons who have been in contact with the patient are not isolated, since the sick are not contagious. The patient's home is disinfected.

Tularemia

What is Tularemia -

Tularemia- an acute infectious 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 ground squirrels that resembled bubonic plague in its clinical picture. 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:

  • Nearctic (African);
  • Central Asian;
  • 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, degree of pathogenicity for humans and animals, sensitivity to certain antibiotics, as well as ecological features 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 temperatures and disinfectants. For disinfection, a 5% phenol solution, a 1:1000 sublimate solution (kills bacteria within 2-5 minutes), 1-2% formalin solution (destroys bacteria for 2 hours), 70° ethyl alcohol, etc. For complete disinfection of the corpses of infected animals, they should be kept for at least 1 day in a disinfectant solution, after which they should be 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 the landscapes of the temperate climate zone of the Northern Hemisphere. The wide distribution of the pathogen in nature, the involvement of a large number of warm-blooded animals and arthropods in its circulation, the contamination of various environmental objects (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 recent years, the incidence has been 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, damage to various organs 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 the clinical classification, the following forms of tularemia are distinguished:

  • 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. Perhaps an isolated or combined lesion of various groups of 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.

Forms of the disease

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, positive symptoms of peritoneal irritation are possible. 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 pneumonic variant is characterized by an acute onset, a sluggish, debilitating course with a 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 remittent, 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, arterial 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:

Differential Diagnosis

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 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, moderate leukocytosis, a neutrophilic shift to the left, and an increase in ESR are noted in the peripheral blood. 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 dynamics of the disease. ELISA on a solid-phase carrier is positive from 6-10 days after the disease, diagnostic titer 1:400; in terms of sensitivity, it is 10-20 times higher than other methods of serological diagnosis of 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 from the inside; the result of the reaction is taken into account after 1-2 days. The test is highly specific and effective already in the early stages (on the 3-5th day) of the disease. 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 with bubo punctate, blood of patients, discharge of the conjunctiva and ulcers, is possible only in special laboratories for working with pathogens of especially 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.

Tularemia Treatment:

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 of normal body temperature. The second row of antibiotics includes third-generation cephalosporins, rifampicin, and levomycetin.

Detoxification therapy is carried out, antihistamines and anti-inflammatory drugs (salicylates), vitamins, cardiovascular agents are indicated. For local treatment of buboes and skin ulcers, ointment dressings, compresses, laser irradiation, and 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. Eliminating the conditions of infection of people (general sanitary and hygienic measures, including sanitary and educational work) has its own characteristics for various types of morbidity. In case of transmissible infections through bloodsuckers, 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). To prevent alimentary infection, swimming in open water should be avoided, and only boiled water should be used for household and drinking purposes. 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 of the ill person is 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.

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Tularemia is an acute infectious natural focal disease, distributed mainly in the Northern Hemisphere in the natural zones of the temperate climate zone. The infection affects human skin, lymph nodes, lungs, mucous membranes of the eyes, throat.

Due to the wide distribution of the causative agent of tularemia in nature, the danger of its entry into the human body can come not only from animals, insects, but also from water and various food products. Adults are more likely to become infected, often this is due to a profession or hobby (fishermen, hunters, agricultural workers, foresters). In men, the disease occurs 3 times more often than in women.

Tularemia was first discovered in 1910 by D. McCoy near Lake Tulare in California. Now, various types of foci of the disease are distinguished: forest, swamp, field, steppe, etc. In places where the focus of infection is spread, it is imperative to be vaccinated against tularemia, it is given to everyone except children under 7 years old. After the first vaccination, the vaccine is re-administered every 5 years, thus reducing the likelihood of an epidemic.

Symptoms of the disease

The incubation period of the disease ranges from 1-30 days, but in the vast majority of cases it is 3-7 days, then the main symptoms appear:

  • An increase in body temperature to 38-39, and sometimes up to 40 ° C.
  • Weakness, increased fatigue.
  • Headache.
  • The fever, which is undulating, can last for weeks.
  • Hyperemia of the face, mucous membrane of the eye and nasopharynx.
  • Rash on the skin.
  • Liver enlargement, splenomegaly.

The method of infection plays a very important role in the manifestation of symptoms of tularemia. If the infection has penetrated the skin (bubonic form), then the lymph nodes are affected - under the armpits, in the groin, etc. The lymph nodes can reach the size of a chicken egg, at first they hurt very much, then the pain subsides, the nodes turn into purulent abscesses, which soon open up.

If the infection occurred in a transmissible way (through mosquito bites, ticks, etc.) - an ulcer-bubonic form, then an ulcer forms at the site of the lesion, which heals very slowly, accompanied by an increase in lymph nodes.

The oculobubonic form occurs when infection occurs through the conjunctiva of the eyes and is characterized by swelling of the eye, acute pain, and foreign body sensation in the eyes. This form is very long and difficult to treat.

When the causative agent of tularemia enters with water or food, an anginal-bubonic form of the disease occurs. There is a sore throat, it is very difficult to swallow, the tonsils swell. The cervical and parotid lymph nodes are enlarged.

When an infection enters the stomach or intestines (abdominal form), severe abdominal pain, diarrhea, and nausea occur. There is an increase in the liver, spleen, with pressure on the navel, there is an increase in pain.

The causative agents of tularemia can enter the human body through the lungs by inhalation of dust (pulmonary form), for example, when threshing cereals. Main symptoms: dry cough, bronchiectasis, chest pain, manifestations of pleurisy.

The generalized form of the disease proceeds as a general inflammatory infection and is characterized by fever, severe headache, splenomegaly, tachycardia, and an increase in ESR.

Causes and causative agent of infection

The cause of tularemia is the ingestion of the causative agent of the disease - the immobile aerobic bacteria Francisella tularensis, which can persist in the environment for a long time, but are not resistant to disinfection, boiling and direct sunlight. Bacteria are divided into 3 types: Nearctic (African), Central Asian and Holarctic (Eurasian).

The main carriers of tularemia are rodents (hares, mice, beavers, rats, etc.), which move a lot and pick up this bacterium. Tularemia is not transmitted from person to person; your family and friends with whom you are in contact are out of danger. The disease occurs when the bacterium enters the body through scratches, burns, damage to the mucous membranes, or through water or food that is contaminated with rodents. Having penetrated the body, the bacteria begin to multiply and settle in various organs, most often in the lungs, spleen, liver, and lymph nodes, which leads to disruption of the normal functioning of these organs.

Diagnostics

When the first symptoms appear, you should consult a doctor. Primary tests (urinalysis, complete blood count, etc.) will show signs of an inflammatory process in the body, a low content of leukocytes in the blood, and an increase in the concentration of monocytes and lymphocytes. At the slightest suspicion of tularemia at an early stage of the disease, the PCR method is used, the reaction of direct agglutination (RA) and indirect hemagglutination (RNHA). On the 5th day after the onset of the disease, it is possible to determine the infection using a skin-allergic test with tularemic toxin. On the 10th day after the onset of the disease, immunofluorescent analysis (ELISA) can be performed, which is the most sensitive method for diagnosing tularemia.

When identifying the method of infection with tularemia, additional diagnostics are carried out - if the infection has got through the eyes, an optometrist is consulted, if through the lungs, an x-ray or computed tomography of the lungs is performed, etc.

Complications

Most often, complications occur with a generalized form of the disease and are manifested by secondary pneumonia. Other possible complications: arthritis, meningitis, inflammation of the heart bag, inflammation of the meninges (meningoencephalitis).

Treatment

Treatment of tularemia is carried out in a hospital. A course of antibiotics is prescribed: streptomycin is administered intramuscularly at 1 g / day and gentamicin 3 times a day at 80 mg. Doxycycline is also prescribed orally 0.2 g / day, sisomicin 0.1 g 3 times a day, kanamycin 0.5 g 4 times a day intramuscularly. Such therapy is carried out until a weekly normalization of body temperature. If there is no significant improvement, then levomycetin, third-generation cephalosporins, rifampicin are used. In the oculobubonic form, albucid-sodium, ointments with antibiotics are prescribed, in the angio-bubonic form - gargling with antiseptics.

At the same time, measures are taken to detoxify the body: antihistamines, salicylates, vitamin complexes are prescribed. Sometimes it becomes necessary to use cardiovascular drugs.

Local treatment of tularemia is carried out with the help of ointment dressings, compresses, sometimes diathermy is used. If the bubo festered, then it is opened and drained.

The prognosis of treatment is favorable. Cases of lethal outcomes are quite rare and are most often observed in the abdominal and pulmonary forms of tularemia.

Prevention

The main measures for the prevention of tularemia are aimed at disinfecting the identified sources of infection, preventing the expansion of the lesion. Particular attention is paid to the observance of sanitary measures at agricultural enterprises, the conduct of deratization and disinfestation, and informing the population about the possible danger of the disease.

Preventive measures should be carried out daily and also include individual protection for each person while hunting (use of protective gloves when butchering a carcass), deratization (wearing overalls), when threshing grain (special aprons, goggles, masks). After completing the above work, be sure to thoroughly wash your hands with soap and water.

It should be remembered that the causative agent of tularemia can enter the human body when drinking water or food, so you should not drink water from a pond, lake or river, especially in areas where the infection is spread.

Specific prophylaxis is also carried out, which consists in vaccinating the population in areas of increased spread of the disease (in the Northern Hemisphere in natural zones of the temperate climate zone). An attenuated vaccine is used, the vaccine gives immunity for 5 years, after which a second vaccination is necessary. The unvaccinated population (seasonal workers, tourists) is restricted from accessing especially dangerous areas (especially with an increase in the number of cases of transmissible infection through mosquitoes or ticks).

With an extremely high probability of infection, emergency prevention of tularemia is carried out - the appointment of a course of antibiotics intramuscularly or intravenously.

Each detected case of the disease is subject to registration and epidemiological study of the source of infection. In the house of a sick person, it is necessary to carry out disinfection measures, and disinfection of the patient’s things with which he has been in contact is also carried out (disinfection of absolutely all the person’s things is not required).



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