Tularemia is a naturally focal acute infection affecting the lymph nodes, skin, and sometimes the mucous membranes of the eyes, pharynx and lungs. Tularemia occurs with pronounced 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, RPH), PCR, skin-allergic test. In the treatment of tularemia, antibacterial, detoxification therapy, surgical autopsy and drainage of suppurated bubons are used.
Tularemia is an acute bacterial infection that occurs with a febrile syndrome, specific lymphadenitis and polymorphic manifestations caused by the entrance gate. Depending on the method of infection, bubonic, ulcerative-bubonic, ocular-bubonic, anginal-bubonic, pulmonary, abdominal and generalized forms of tularemia are isolated. Foci of tularemia are found in many countries of the northern hemisphere. Along with the plague, cholera, anthrax and other infections, tularemia is classified as a particularly dangerous infection.
Clinical classification of tularemia is made depending on the localization of infection (bubonic, ulcerative-bubonic, oculobubonic, angiotic-bubonic, abdominal and generalized tularemia), duration (acute, prolonged and recurrent) and severity (mild, moderate and severe).
Characteristics of the pathogen
The causative agent of tularemia is the aerobic gram-negative rod bacterium Francisella tularensis. 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 (hares, dogs, sheep, etc.) The greatest contribution to the spread of infection is made by rodents (vole, muskrat, etc.). A sick person is not contagious. The most common transmissive transmission mechanism. The microbe enters the body of animals when bitten by a tick or blood-sucking insects. Tularemia is characterized by infection of animals when bitten by an ixod mite. A person becomes infected by contact with sick animals (skinning, collecting rodents) or by eating food and water infected with animals.
The respiratory route of transmission of infection is realized by inhaling dust from bacteria-infected grain or straw, in agricultural production (processing of vegetable raw materials, meat processing plants, slaughter of cattle, etc.). Despite the low probability of infection with tularemia outside the natural focus of the pathogen, it is possible to get sick when in 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 infected people.
The incubation period of tularemia can be from one day to a month, but most often it is 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 remitting, but it can also be constant, intermittent or wave–like (two or three waves). The duration of the fever can range from a week to two to three months, but is usually 2-3 weeks.
On examination, there is hyperemia of the face, conjunctiva and mucous membranes of the oral cavity, nasopharynx, pasty, injection of sclera. In some cases, exanthema (skin rash) of various types is detected. 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 method of infection. If the entrance gate of infection is the skin, the bubonic form develops, which is regional lymphadenitis. Axillary, inguinal, femoral lymph nodes may be affected, with further spread, secondary bubones may be noted.
The affected lymph nodes are enlarged in size (sometimes reaching the size of a chicken egg), with distinct contours, initially painful, then the pain decreases and subsides. Gradually, the bubones dissolve (often within a few months), sclerose or build up, forming abscesses, which are then opened onto the skin with the formation of a fistula.
The ulcerative bubonic form usually develops with a 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. Regional lymphadenitis develops in parallel.
When the pathogen penetrates through the conjunctiva, tularemia manifests itself in the form of an ocular bubonic 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 into erosion and ulcers with purulent discharge. The cornea is usually not affected. This form of tularemia often proceeds very hard and for a long time.
The anginous-bubonic form occurs if the pharyngeal mucosa serves as the gateway of infection, infection occurs through the consumption of contaminated food and water. It is clinically manifested by sore throat, dysphagia (difficulty swallowing), hyperemia and swelling of the tonsils are noted during examination. On the surface of enlarged tonsils, soldered to the surrounding tissue, a grayish, hardly removable necrotic plaque is often visible. With the progression of the disease, the tonsils necrotize, forming ulcers with difficulty healing and, later, scars. Lymphadenitis in this form of tularemia occurs in the parotid, cervical and submandibular nodes from the affected amygdala.
When an infection of the lymphatic vessels of the mesentery of the intestine is affected, tularemia manifests itself in the form of an abdominal clinical form, severe abdominal pain, nausea (sometimes vomiting), anorexia. Diarrhea may occur. Palpation soreness is localized in the navel area, hepatosplenomegaly is noted.
The pulmonary form of tularemia (which develops when inhaling dust containing bacteria) occurs in two clinical variants: bronchitic and pneumonic. The bronchitic variant (with the defeat of 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, the formation of abscesses, cavities, up to pulmonary gangrene.
The generalized form proceeds according to the type of typhoid and paratyphoid infections or sepsis. Fever is improperly remitting, long-lasting, intoxication is pronounced, intense muscle pain, progressive weakness, headache, dizziness, delirium, hallucinations, confusion.
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 and toxic shock is possible. Sometimes tularemia can be complicated by meningitis and meningoencephalitis, inflammation of the heart sac, arthritis.
Non-specific laboratory techniques (general analysis of blood, urine) show signs of inflammation and intoxication. In the first days of the disease there is neutrophilic leukocytosis in the blood, in the future the total number of leukocytes decreases, the concentration of fractions of lymphocytes and monocytes increases.
Specific serological diagnostics is performed with the help of RPH (reactions of direct agglutination and indirect hemagglutination). With the progression of the disease, the titer of specific antibodies increases. From 6-10 days after the onset of the disease, it is possible to determine tularemia using immunofluorescence analysis (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 with the help of a skin-allergic test with tularemictoxin (gives the result already on the 3-5 day of the disease).
Since the isolation of bacteria from blood and other biological materials is a certain difficulty, bacteriological seeding is rarely carried out. On the 7th-10th day of the disease, it is possible to isolate the causative agent by back-sowing the separated ulcers, punctate of bubones, but the laboratory tools necessary for sowing this culture are not widespread. In the pulmonary form of tularemia, radiography or lung CT scan is performed.
Tularemia is treated in a hospital with an infectious profile, discharge is made after full recovery. Specific therapy of tularemia consists in prescribing a course of antibiotics: streptomycin with gentomycin intramuscularly. In addition, other broad-spectrum antibiotics (doxycycline, kanamycin) can be used. 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 with intravenous infusion solutions for detoxification), anti-inflammatory and antipyretic agents (salicylates) and antihistamines, vitamins. If necessary – cardiovascular products. Skin ulcers are covered with sterile bandages, suppurated bubons are opened and drained.
Prevention of tularemia includes measures to decontaminate sources of spread, to prevent transmission routes. Of particular importance in preventive measures is the sanitary and hygienic condition of food and agriculture enterprises in areas endemic to this pathogen, deratization and disinsection.
Individual measures of protection against infection are necessary when hunting wild animals (skinning, butchering), deratization (when collecting poisoned rodents). Hands should preferably be protected with gloves, or thoroughly disinfected after contact with animals. As a suppression of the alimentary transmission route, it is advisable to avoid drinking water from an unreliable source without special treatment.
Specific prevention of tularemia is vaccination of the population in endemic areas with a live tularem vaccine. Immunity is formed for 5 or more (up to seven) years. Revaccination in 5 years. Emergency prevention (with a high probability of infection) is carried out by intravenous administration of antibiotics. When identifying a patient with tularemia, only those things that were used in contact with an animal or infected raw materials are subject to disinfection.