Causes and pathogenesis of legionellosis

Cause of Legionellosis

Legionellosis is caused by Legionella ofthe Legionellaceae family, discovered in 1977 by D. McDaid and S. Shepard. Legionella are gram-negative, motile coccobacillary bacteria with flagella and fimbriae. They do not form spores. They have intracellular vacuoles and numerous ribosomes. The presence of internal and external membranes is characteristic. The nucleoid is diffusely distributed in the cytoplasm. Genomic DNA has a molecular weight of 2.5x10 ⁹ Da. Legionella are facultative intracellular parasites with a complex enzymatic system, the activity of which depends on the culture medium and habitat conditions. The antigenic structure is complex, the main antigens are type- and group-specific. According to antigens, legionella are divided into at least eight serogroups. There is an antigenic relationship between I. pneumophilla and Chlamydia psittaci. Pathogenicity factors are a heat-stable, protein-polysaccharide endotoxin with hemolytic activity, and cytolysin with cytotoxic and proteolytic action.

Legionella are resistant to physical and chemical factors, sensitive to ultraviolet radiation, antibiotics (macrolides, rifampicin, fluoroquinolones, chloramphenicol). Penicillin and cephalosporins do not affect the pathogen.

Pathogenesis of legionellosis

The entry point for the pathogen is the mucous membrane of the respiratory tract, including lung tissue. The size of aerosol particles, the aerodynamic characteristics of the air flow, and the characteristics of the patient's external respiration determine the different probability of infection. There is data on the possibility of the pathogen entering the blood, tissue fluid with subsequent development of infection during medical manipulations, surgical interventions in people with immunodeficiency.

The most severe course of legionellosis in the form of acute alveolitis is observed in cases where the infectious dose is high and the diameter of aerosol particles does not exceed 2-2.5 μm (this allows them to reach the alveoli). Legionella, having overcome the barrier of the ciliated epithelium, are carried into the bronchioles and alveolar ducts, and can directly penetrate the cells of the alveolar epithelium. However, in most cases, mobilization of a protective cellular shaft around the penetrated legionella is observed. In this case, microorganisms are detected in alveolar macrophages, monocytes, and polymorphonuclear neutrophils. With electron microscopy, legionella can be detected both intra- and extracellularly.

Legionellosis lung lesions are accompanied by the involvement of blood vessels in the process. This causes microcirculation disorders up to the development of respiratory distress syndrome. In legionellosis, which occurs as an acute respiratory infection-like syndrome, acute tracheitis or bronchitis, the majority of microorganisms do not pass the ciliary system barrier or are retained for a long time in the mucous membrane of the trachea and bronchi. This activates defense mechanisms, including macrophages. Individual microorganisms that reach the terminal bronchioles and alveolar ducts undergo active phagocytosis, while there is no pronounced infiltration characteristic of the inflammatory process. Lung pathology begins with bronchitis and bronchiolitis with the rapid formation of lobular foci of inflammation, often merging. This leads to lobar, often bilateral lung lesions in the form of pleuropneumonia, macroscopically similar to gray and red hepatization of the lung in pneumococcal pneumonia. Lung lesions in severe cases of the disease often end in obliteration. Dissemination of the pathogen occurs lymphogenously through the septal lymphatic vessels. Through regional lymph nodes, microorganisms enter the blood, resulting in bacteremia.

Legionella can be carried hematogenously to organs and involve them in the pathological process. Endotoxin causes systemic lesions. In severe cases, infectious toxic shock develops with acute multiorgan, primarily respiratory failure, renal and hepatic failure and acute hepatic encephalopathy. CNS damage is caused by the entry of toxins into the blood with the rapid death of the microorganism in the lesion. Renal tubular cells are sensitive to the toxic effects of legionella and often become necrotic. The toxic effect on the hepatocyte increases the activity of aminotransferases and the concentration of bilirubin in the blood. Under the influence of the toxin, as a result of damage to the bone marrow, hematopoiesis processes are inhibited.

Thus, the pathogenesis of legionellosis includes phases of bronchogenic, lymphogenic and hematogenous development of the infectious process. Extrapulmonary lesions occur hematogenously. In this case, the development of generalized septic forms is possible, in particular, septic endocarditis.

Epidemiology of legionellosis

Legionellosis is widespread. The disease is registered both in the form of outbreaks and sporadic cases on all continents of the globe. According to some data, in the etiological structure of pneumonia, legionella accounts for 10%, and among atypical pneumonia - about 25%. The carriage of pathogens in birds, rodents, arthropods has not been established. Legionella are natural inhabitants of reservoirs, capable of existing in various environmental conditions. They can be isolated from the air and natural waters, where the bacteria grow in association with blue-green algae (presumably they are able to live inside seaweed and free-living amoebas). In unchlorinated drinking water, they persist for more than 1 year. Irrigation systems, sprinklers, shower heads, air conditioners, inhalers, excavation work pose a certain epidemic hazard.

At present, the only confirmed route of transmission of the infection is airborne. The factors of transmission of the infection are water and soil in endemic areas,water in recirculating air conditioning systems, as well as in water supply systems.

Legionellosis is characterized by a clearly expressed seasonality (summer-autumn). More frequent registration of infection in the summer months can explain the more intensive use of air conditioning systems, which often serve as a reservoir of the pathogen.

Men are twice as likely to get sick as women. The disease is more common in middle-aged and elderly people.

Infection without pneumonia of the ARI type is more often diagnosed in younger people. Risk factors predisposing to the development of the disease are immunodeficiency states, smoking, alcohol abuse, and living near excavation sites.

In recent years, particular importance has been attached to the problem of so-called travel-associated legionellosis. A unified international system of epidemiological control over cases of legionellosis associated with tourist and business trips has been created.

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