Infectious diseases. Diphtheria. Etiology. Epidemiology. Pathogenesis and pathomorphology (most important)

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Infectious diseases. Diphtheria. Etiology. Epidemiology. Pathogenesis and pathomorphology (most important)

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26. Diphtheria. Etiology. Epidemiology. Pathogenesis and pathomorphology

Diphtheria is an acute infection caused by Corynеbacterium diphtheriae, the symptoms of which are due to the production of a toxin - an extracellular protein product of a toxigenic strain of the pathogen.

Etiology. The causative agent of diphtheria, Corynebacterium diphtheriae, or Leffler's bacillus, is an unevenly stained gram-positive, non-spore-bearing, immobile pleomorphic bacterium.

Toxigenic and non-toxigenic microorganisms are found among smooth and rough strains, the production of exotoxin is determined in any of the three types of Corynebacterium colonies.

Diseases are caused by toxigenic and non-toxigenic strains of diphtheria bacillus, but only the first, toxigenic, are responsible for the development of complications such as myocarditis and neuritis.

Epidemiology. Infection occurs through contact with a sick person or a carrier. Bacteria are transmitted by airborne droplets, the role of the household route of infection is small.

Pathogenesis and pathomorphology. Initially, the infection is localized on the mucous membranes of the upper respiratory tract, less often on the conjunctival membrane, wound surfaces of the skin or in the genital area. After 2-4 days of the incubation period, the strains of the pathogen with the bacteriophage begin to produce a toxin, which is first adsorbed on the cell wall, then overcomes it and interferes with the processes of protein synthesis of the cell.

Tissue necrosis is most pronounced along the periphery of the breeding zones of diphtheria pathogens. In these areas, an inflammatory reaction develops, which, together with the processes of necrosis, contributes to the formation of characteristic plaques, which are initially easily removed. As toxin production increases, the affected area becomes wider and deeper, fibrinous deposits appear on its surface, quickly transforming into dense, firmly fixed films from gray to black, depending on the blood content in them. They also include fibrin and surface epithelial cells. The separation of the film causes bleeding, since the epithelial layer is firmly included in its composition. In the process of recovery, the films peel off on their own.

Swelling of the surrounding soft tissues can become rampant. Films and edematous soft tissues can hang over the airways, disrupting their patency and causing suffocation, which may be accompanied by expansion of the larynx and tracheobronchial tree.

The toxin formed at the breeding site of diphtheria bacilli enters the bloodstream and spreads throughout the body. When the tonsils, pharynx and pharynx are already covered with diphtheria films, toxemia begins.

The toxin has a destructive effect most of all on the heart, nervous system and kidneys. After fixation of the toxin in the cells, a latent period passes before the development of clinical symptoms. Myocarditis usually develops in 10-14 days, and diseases of the nervous system - not earlier than 3-7 weeks after the onset of the disease.

Author: Pavlova N.V.

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