Mycoplasmosis (mycoplasmal infection) - Causes and pathogenesis

Mycoplasmas are bacteria of the Mollicutes class: the causative agent of respiratory mycoplasmosis is mycoplasma of the Pneumoniae species of the Mycoplasma genus . The absence of a cell wall determines a number of properties of mycoplasmas, including pronounced polymorphism (round, oval, filiform shapes) and resistance to beta-lactam antibiotics. Mycoplasmas reproduce by binary fission or due to desynchronization of cell division and DNA replication, they elongate with the formation of filiform, mycelial forms containing a repeatedly replicated genome and subsequently dividing into coccoid (elementary) bodies. The size of the genome (the smallest among prokaryotes) determines the limited possibilities of biosynthesis and, as a consequence, the dependence of mycoplasmas on the host cell, as well as 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 connection with the membrane of eukaryotic cells. The 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 the cells of the macroorganism. Mycoplasmas may exist 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 hemadsorption).

Mycoplasmas are unstable in the environment: in aerosols in indoor conditions they remain viable for up to 30 minutes, they die under the influence of ultraviolet rays, disinfectants, are sensitive to changes in osmotic pressure and other factors.

Epidemiology of mycoplasmosis (mycoplasma infection)

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

The transmission mechanism is aspirational, carried out mainly by airborne droplets. For the transmission of the pathogen, fairly close and prolonged contact is necessary.

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

The duration of post-infectious immunity depends on the intensity and form of the infectious process. After mycoplasma pneumonia, pronounced cellular and humoral immunity is formed lasting 5-10 years.

M. pneumoniae infection is widespread, but the greatest number of cases is observed in cities. Respiratory mycoplasmosis is not characterized by: rapid epidemic spread, typical of respiratory viral infections. Transmission of the pathogen requires fairly close and prolonged contact, so respiratory mycoplasmosis is especially common in closed groups (military, student, etc.); in newly formed military groups, up to 20-40% of pneumonias are 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.

Secondary cases of M. pneumoniae infection in family foci are typical (a school-age child becomes ill initially); they develop in 75% of cases, with the transmission rate reaching 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 periods: outbreaks of respiratory mycoplasmosis occur more often in the autumn.

M. pneumoniae infection is characterized by a periodic increase in morbidity at intervals of 3-5 years.

Specific prevention of mycoplasmosis has not been developed.

Non-specific prevention of respiratory mycoplasmosis is similar to prevention of other acute respiratory infections (separation, wet cleaning, ventilation of premises).

Pathogenesis of mycoplasmosis (mycoplasma infection)

M. pneumoniae gets on the surface of the mucous membranes of the respiratory tract. It penetrates the mucociliary barrier and firmly attaches to the membrane of epithelial cells using terminal structures. Parts of the pathogen membrane are embedded in the cell membrane; close intermembrane contact does not exclude the penetration of mycoplasma contents into the cell. Intracellular parasitism of mycoplasmas is possible. Damage to epithelial cells due to the use of cellular metabolites and sterols of the cell membrane by mycoplasmas, as well as due to the action of mycoplasma metabolites: hydrogen peroxide (hemolytic factor M, pneumoniae) and superoxide radicals. One of the manifestations of damage to the cells of the ciliated epithelium is dysfunction of the cilia up to ciliostasis. which leads to disruption of mucociliary transport. Pneumonia caused by M. pneumoniae is often interstitial (infiltration and thickening of the interalveolar septa, the appearance of lymphoid histiocytic and plasma cells in them, damage to the alveolar epithelium). There is an increase in peribronchial lymph nodes.

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

Respiratory mycoplasmosis is highly characterized by the formation of cold agglutinins. It is assumed that M. pneumoniae affects the erythrocyte antigen I, making it an immunogen (according to another version, their epitopic relationship is not excluded), as a result of which complement-binding cold IgM antibodies to the erythrocyte antigen I are produced.

M. pneumoniae causes polyclonal activation of B and T lymphocytes. Infected individuals show a significant increase in total serum IgM levels.

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

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