Children's infectious diseases. Tularemia (lecture notes)

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Children's infectious diseases. Tularemia (lecture notes)

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Lecture number 11. Tularemia

Tularemia - a typical zoonosis, is a natural focal infectious disease that occurs with symptoms of general intoxication, fever and the development of specific lymphadenitis, less often without pronounced disorders. The causative agent is Francisella tularensis (Pasteurella tularensis).

Clinical manifestations of this infection depend on the virulence of the pathogen and the route of infection. There are five clinical forms of the disease: ulcerative glandular (80% of all cases of this infection), glandular (10%), ophthalmic (1%), typhoid (almost 6%). The incidence of tularemia pharyngitis and pneumonia in children remains unknown, but oropharyngeal forms occur.

Etiology. The causative agent of tularemia is a short, gram-negative, non-motile bacterium that does not have a capsule and does not form spores. When grown on nutrient media, bacteria exhibit pronounced signs of polymorphism. Working with pathogen cultures requires special care due to the risk of infection.

F. tularensis strains are antigenically homogeneous, but their virulence is very different: type A strain Jellison is highly virulent for humans, type B of this strain causes only mild forms of the disease in humans.

Epidemiology. The causative agent of tularemia has been isolated from one hundred different species of mammals and arthropods. Type A bacteria are commonly found in white-tailed rabbits and ticks. Type B is more typical for rats, mice, squirrels, beavers, nutmeg rats, moles, birds and the ticks that parasitize them. Tularemia is transmitted by fleas, lice, mosquitoes and horseflies.

Tularemia most often develops in hunters, cooks, fur breeders and other persons who, by the nature of their occupations, most often encounter the pathogen.

The disease can occur in children who consume contaminated food (rabbit meat or proteins) or water. Often the disease occurs after being bitten by infected ticks, mosquitoes, or other carriers of the disease.

Pathomorphology and pathogenesis. A person becomes infected with tularemia when the pathogen penetrates through damaged or healthy skin, mucous membranes, through an insect bite, through the lungs or gastrointestinal tract. After 48-72 hours, an erythematous, maculopapular formation appears on the skin at the site of bacterial penetration, quickly ulcerating, and local lymphadenopathy. The pathogen multiplies in the lymph nodes and causes the formation of granulomas in them. Subsequently, bacteremia may develop, leading to damage to a variety of organs. However, the most pronounced changes occur in the reticuloendothelial system.

With the inhalation route of infection, bronchopneumonia develops, less often lobar pneumonia. Inflammatory changes are localized in the places where bacteria settle, accompanied by necrosis of the walls of the alveoli. In some cases, bronchitis rather than pneumonia may occur after inhalation exposure.

The causative agent of tularemia, which has entered the lungs, is phagocytosed by alveolar macrophages and enters with them into the lymph nodes of the root of the lungs, and from there into the general circulation. Typhoid forms of tularemia are caused by aspiration of chewed contaminated food.

The factors that determine the virulence of the causative agent of tularemia have not yet been studied. F. tularensis does not produce exotoxin, and no relationship between virulence and antiphagocytic activity of individual strains of these bacteria was noted.

The causative agent of tularemia is an intracellular parasite that can persist for a long time in monocytes and other cells of the macroorganism, which creates the risk of a chronic course and subsequent exacerbations of the infection.

Cellular immunity responses may be of great importance in resistance to tularemia, the role of circulating antibodies is less prominent.

Clinical manifestations. The incubation period for tularemia varies from several hours to 1 week. The disease begins acutely with an increase in body temperature to 40-41 °C, chills, muscle and joint pain, nausea, vomiting and sweating. Headaches are often very severe, but in young children they are usually absent. Sometimes photophobia is observed, and a maculopapular rash appears. Moderate anemia may develop. The number of leukocytes in peripheral blood may be within normal limits, increased or decreased, and ESR may not change. Transient proteinuria is observed.

The primary changes on the skin in the ulcerative-glandular form of tularemia during the first 3 days are maculopapular in nature. By the 4-5th day of illness, they ulcerate and become painful. Healing occurs within 4 weeks. Lymphangitis around the ulcers is usually absent. Enlarged regional lymph nodes are dense, sensitive, in 25% of cases, if left untreated, they melt. Some patients have generalized enlargement of the lymph nodes and splenomegaly.

The oropharyngeal form of tularemia is characterized by the development of purulent tonsillitis and pharyngitis, and sometimes ulcerative stomatitis. The general manifestations of the disease are the same as in the ulcerative glandular form.

The glandular form of tularemia does not differ from the ulcerative glandular, a characteristic feature is the absence of changes in the skin and mucous membranes. The oculoglandular form of tularemia is similar to the cutaneous glandular one, but the primary lesion in it is represented by severe conjunctivitis and an increase in regional lymph nodes.

The typhoid form of tularemia resembles typhus. The febrile state is kept for a long time, changes on the skin and mucous membranes may be absent. There are dry cough, severe chest pain, hemoptysis. The clinical picture of bronchitis, pneumonitis or pleurisy is observed in 20% of patients. In most patients in these cases, X-ray examination reveals the involvement of lung tissue and pleura in the process, an increase in the lymph nodes of the lung root. Often note splenomegaly, sometimes an increase in the liver.

Cases of the development of meningitis, encephalitis, pericarditis, endocarditis, neuralgia, thrombophlebitis and osteomyelitis are described.

Diagnosis. For the diagnosis of tularemia, the following are of great importance:

1) allergic (intradermal, dermal) test with tularin, which is put according to the type of Pirquet and Mantoux reactions. The reaction is recorded after 1-2 days and is considered positive in the presence of infiltrate and hyperemia of at least 0,5 cm;

2) serological RA with high specificity, but the late appearance of agglutinins in the blood reduces their value as an early diagnostic method; as well as RPHA and ROP - strictly specific and reliable for the diagnosis of tularemia and the retrospective diagnosis of this infection;

3) bacteriological diagnostic methods (they are of additional importance and are not always effective).

Differential diagnosis. The ulcerative-glandular form of tularemia is differentiated from cat scratch disease, infectious mononucleosis, sporotrichosis, plague, anthrax, melioidosis, glanders, rat bite fever, or lymphadenitis caused by streptococcus pyogenes or Staphylococcus aureus. The oropharyngeal form of tularemia is differentiated from the same diseases and from acquired cytomegalovirus infection and toxoplasmosis, adenoviral infection and herpes simplex.

Pneumonitis in tularemia is differentiated from other bacterial and non-bacterial pneumonias, especially those caused by mycoplasmas, chlamydia, mycobacteria, fungi and rickettsiae. Their exact differentiation is possible only when the pathogen is isolated.

The typhoid form of tularemia is differentiated from typhoid, brucellosis and other diseases accompanied by septicemia.

Treatment. Positive results are obtained with treatment with streptomycin, as well as tetracycline and chloramphenicol, however, when treating the latter, relapses often occur, requiring repeated courses of treatment with tetracycline.

Forecast. Death in untreated ulcerative glandular form of tularemia occurs in 5% of cases. If untreated, the disease lasts 2-4 weeks, and within 8-12 weeks there is a decrease in performance.

Pneumonia, both primary and secondary, developed against the background of the bubonic form of tularemia, ends in death in 30% of patients who did not receive appropriate therapy. Those who recover from tularemia acquire immunity to it for life. Relapses are rare and mild. The disease caused by the Jellison type B strain is characterized by a milder course. Properly performed treatment provides a quick and complete cure, while deaths are extremely rare.

Prevention. The main method of prevention is vaccination using the live attenuated anti-tularemia vaccine Elbert-Gaisky. In tularemia-endemic areas and adjacent areas, routine vaccinations cover the entire population over 7 years of age, and in some cases, children under 2 years of age.

In the tularemia focus, a complex of sanitary and anti-epidemic measures is carried out, regulated by a special decree.

Author: Muradova E.O.

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