Causes and pathogenesis of legionellosis

The reason of legionellosis

Legionellosis is caused by Legionella family Legionellaceae was discovered in 1977 by D. McDead and S. Shepard. Legionella are gram-negative, mobile coccobacillary bacteria that have flagella and pili. The dispute does not form. They have intracellular vacuoles and a lot of 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 2.5 × ^{10 9} Da. Legionella are facultative intracellular parasites with a complex enzymatic system whose activity depends on the culture medium and habitat conditions. The antigenic structure is complex, the main antigens are type- and group-specific. At antigens, legionella is secreted by at least eight serogroups. They have an antigenic relationship between I. pneumophilla and Chlamydia psittaci. Pathogenicity factors are thermostable, protein-polysaccharide endotoxin, which has hemolytic activity, and cytolysin with cytotoxic and proteolytic action.

Legionellae are resistant to the action of physical and chemical factors, sensitive to ultraviolet radiation, to antibiotics (macrolides, rifampicin, fluoroquinolones, chloramphenicol). Penicillin and cephalosporins do not act on the pathogen.

Pathogenesis of Legionellosis

The entrance gate of the pathogen of infection is the mucous membrane of the respiratory tract, including the lung tissue. The dimensions of aerosol particles, aerodynamic characteristics of the air flow, and also the peculiarities of the patient's external respiration determine a different probability of infection. There are data on the possibility of the causative agent entering the bloodstream, the tissue fluid, followed by the development of infection during medical manipulations, surgical interventions in persons with immune deficiency.

The heaviest legionellosis in the form of acute alveolitis is observed in cases when the infecting dose is high and the particle diameter of the aerosol does not exceed 2-2.5 μm (this allows them to reach the alveoli). Legionella, breaking the barrier of the ciliated epithelium, are entered into the bronchioles and alveolar ducts, can directly penetrate into cells of the alveolar epithelium. However, in most cases, mobilization of the protective cell shaft around the introduced 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.

Legionella infections of the lungs are accompanied by the involvement of vessels in the process. This causes disturbances in microcirculation up to the development of respiratory distress syndrome. With legionellosis. Occurring in the form of an acute respiratory syndrome-like syndrome, acute tracheitis or bronchitis, the majority of microorganisms do not pass the barrier of the ciliary system or stay in the mucous membrane of the trachea and bronchi for a long time. This activates protective mechanisms, including macrophages. Individual microorganisms reaching the terminal bronchioles and alveolar ducts undergo active phagocytosis, and there is no pronounced infiltration characteristic of the inflammatory process. The pathology of the lungs begins with bronchitis and bronchiolitis with the rapid formation of the lobular foci of inflammation, often merging. This leads to shared, often bilateral lung lesions in the form of pleuropneumonia, macroscopically similar to the gray and red cuff of the lung in pneumococcal pneumonia. The defeat of the lungs during a severe course of the disease often ends with subscription. Dissemination of the pathogen occurs lymphogenically through septal lymphatic vessels. Through regional lymph nodes, microorganisms enter the bloodstream, resulting in bacteremia.

Legionella can be hematogenously transmitted to organs and involve them in the pathological process. Endotoxin causes systemic lesions. In severe cases, an infectious-toxic shock develops acute polyorganic, primarily respiratory failure, renal-hepatic insufficiency and acute hepatic encephalopathy. The defeat of the central nervous system is due to the introduction of toxins into the blood with rapid death of the microorganism in the lesion. To the toxic effect of Legionella sensitive cells of the renal tubules are sensitive, which are often necrotic. The toxic effect on the hepatocyte increases the activity of aminotransferases and the concentration of bilirubin in the blood. Under the influence of toxin as a result of damage to the bone marrow, processes of hematopoiesis are inhibited.

Thus, the pathogenesis of legionellosis includes the phases of bronchogenic, lymphogenic and hematogenous development of the infectious process. Extrapulmonary damage occurs hematogenically. It is possible to develop generalized septic forms, in particular, septic endocarditis.

Epidemiology of legionellosis

Legionellosis is common everywhere. The disease is recorded both in the form of outbreaks and sporadic cases on all continents of the globe. According to some data, the proportion of legionella in the etiological structure of pneumonia is 10%, and among atypical pneumonia - about 25%. Carrying out pathogens in birds, rodents, arthropods is not established. Legionella are natural inhabitants of reservoirs, able to exist in various environmental conditions. They can be isolated from air and natural waters, where bacteria grow in association with blue-green algae (presumably they are able to live inside seaweed and free-living amoebae). In non-chlorinated drinking water are stored for more than 1 year. A certain epidemic danger is represented by irrigation systems, sprinklers, shower heads, air conditioners, inhalers, earthworks.

At present, the only confirmed way of transmission of infection is aerogenic. Transmission factors are water and soil in endemic areas, water in air-conditioning systems of recirculating type, as well as in water supply systems.

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

Men are sick twice as often as women. More often this disease is met in middle-aged and elderly people.

Infection without pneumonia by type of acute respiratory infections is more often diagnosed in persons of younger age. Risk factors predisposing to the onset of the disease are immunodeficiency, smoking, alcohol abuse, and living near excavation sites.

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

[1], [2], [3], [4], [5], [6], [7],