Mycoplasmosis (mycoplasma infection): causes and pathogenesis

Mycoplasmas are Mollicutes class bacteria : an agent of respiratory mycoplasmosis is mycoplasma of the species Pneumoniae of the genus Mycoplasma. The absence of the cell wall causes a number of properties of mycoplasmas, including pronounced polymorphism (rounded, oval, filiform forms) and resistance to beta-lactam antibiotics. Mycoplasmas multiply by binary fission, or due to desynchronization of cell division and DNA replication, extend to form filamentous, mycelial-like forms that repeatedly replicate with the genome and subsequently separate into coccoid (elementary) bodies. The size of the genome (the smallest among the prokaryotes) determines the limited possibilities of biosynthesis and, as a consequence, the dependence of mycoplasmas on the host cell, as well as the high requirements for nutrient media for cultivation. Cultivation of mycoplasmas is possible in tissue culture.

Mycoplasmas are widespread in nature (they are isolated from humans, animals, birds, insects, plants, soil and water).

Mycoplasmas are characterized by a close relationship with the membrane of eukaryotic cells. Terminal structures of microorganisms contain proteins p1 and p30, which probably play a role in the mobility of mycoplasmas and their attachment to the surface of cells of the macroorganism. Perhaps the existence of mycoplasmas inside the cell, which allows them to avoid the effects of many protective mechanisms of the host organism. The mechanism of damage to the cells of the macroorganism is multifaceted (M. Pneumoniae, in particular, produces hemolysin and has the ability to gemadsorption).

Mycoplasmas are not very stable in the environment: as a part of the aerosol, in the conditions of the room, they remain viable for up to 30 minutes, die under the action of ultraviolet rays, disinfectants, and are sensitive to changes in osmotic pressure and other factors.

Epidemiology of mycoplasmosis (mycoplasmal infection)

The source of the pathogen is a sick person with a manifest or asymptomatic form of M. Pneumoniae infection (it can be secreted from pharyngeal mucus for 8 weeks or more from the onset of the disease even in the presence of antimycoplasmic antibodies and despite effective antimicrobial therapy). Transient carrier M. Pneumoniae is possible.

The mechanism of transmission is aspiration, carried out mainly by airborne droplets. To transmit the pathogen requires a fairly close and long-term contact.

Susceptibility to infection is highest in children aged 5 to 14 years, among adults, the most affected age group is those under the age of 30-35.

The duration of postinfection immunity depends on the intensity and form of the infectious process. After the transferred mycoplasmal pneumonia, a pronounced cellular and humoral immunity with a duration of 5-10 years is formed.

M. Pneumonia infection is ubiquitous, but the greatest number of cases are seen in cities. For respiratory mncoplasmosis, not the characters: rapid epidemic spread, characteristic of respiratory viral infections. To transmit the pathogen requires a fairly close and long-term contact, so respiratory mycoplasmosis is especially common in closed collectives (military, student, etc.); in newly formed military collectives up to 20-40% of pneumonia is caused by M. Pneumoniae. Against the background of sporadic morbidity, outbreaks of respiratory mycoplasmosis are periodically observed in large cities and closed groups, lasting up to 3-5 months or more.

Typical secondary cases of M. Pneumoniae infection in family foci (the primary school child is ill); they develop in 75% of cases. While the transmission rate reaches 84% in children and 41% in adults.

Sporadic incidence of M. Pneumoniae infection is observed throughout the year with some increase in the autumn-winter and spring period: outbreaks of respiratory mycoplasmosis occur more often in the autumn.

For M. Pneumoniae infection is characterized by a periodic increase in the incidence of disease with an interval of 3-5 years.

Specific prophylaxis of mycoplasmosis has not been developed.

Nonspecific prevention of respiratory mycoplasmosis is similar to the prevention of other ARI (separation, wet cleaning, ventilation of premises).

Pathogenesis of mycoplasmosis (mycoplasmal infection)

M. Pneumoniae falls on the surface of the mucous membranes of the respiratory tract. Penetrates the mucociliary barrier and is firmly attached to the membrane of epithelial cells by means of terminal structures. Incorporation of the sections of the exciter membrane into the cell membrane takes place; close intermembranous contact does not exclude the penetration of the contents of mycoplasmas into the cell. Perhaps intracellular parasitization of mycoplasmas. Damage to epithelial cells due to mycoplasma use of cellular metabolites and cell membrane sterols, and also due to the action of mycoplasma metabolites: hydrogen peroxide (hemolytic factor M, pneumoniae) and superoxide radicals. One of the manifestations of the defeat of cells of the ciliated epithelium is dysfunction of the cilia down to ciliostasis. Which leads to a violation of mucociliary transport. Pneumonia caused by M. Pneumoniae, often interstitial (infiltration and thickening of interalveolar septa, appearance of lymphoid histiocytic and plasma cells in them, defeat of alveolar epithelium). There is an increase in peribronchial lymph nodes.

In the pathogenesis of mycoplasmosis, great importance is attached to immunopathological reactions, which probably causes many extrapulmonary manifestations of mycoplasmosis.

For respiratory mycoplasmosis, the formation of Cold agglutinins is highly characteristic. It is assumed that M. Pneumoniae affects the antigen of erythrocytes I, making it an immunogen (according to another version, their epitope kinship is possible), resulting in the production of complement-binding cold IgM antibodies to the erythrocyte I. Antigen.

M. Pneumoniae causes polyclonal activation of B- and T-lymphocytes. In infected, the level of total serum IgM is significantly increased.

M. Pneumoniae induces a specific immune response, accompanied by the production of secretory IgA and circulating IgG antibodies.

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