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Causes and pathogenesis of pneumococcal infection
Last reviewed: 06.07.2025

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Causes of pneumococcal infection
According to the modern classification, pneumococci belong to the Streptococcaceae family, Streptococcus genus . These are gram-positive cocci of oval or spherical shape, 0.5-1.25 µm in size, located in pairs, sometimes in short chains. Pneumococci have a well-organized capsule. According to its polysaccharide composition, more than 85 serotypes (serovars) of pneumococci have been identified. Only smooth capsular strains are pathogenic for humans, which, using special serums, are classified as one of the first 8 types; the remaining serovars are weakly pathogenic for humans.
When pneumococci are destroyed, endotoxin is released.
Pathogenesis of pneumococcal infection
Pneumococci can affect any organs and systems, but the lungs and respiratory tract should be considered a triple organ. The reasons that determine the tropism of pneumococci to the bronchopulmonary system have not been reliably established. It is more likely that the capsular antigens of pneumococci have an affinity for lung tissue and the epithelium of the respiratory tract. The introduction of the pathogen into the lung tissue is facilitated by acute respiratory infections, which eliminate the protective function of the epithelium of the respiratory tract and reduce the overall immunoreactivity. Various congenital and acquired defects of the bacterial antigen elimination system are also important: defects of the surfactant system of the lung, insufficient phagocytic activity of neutrophils and alveolar macrophages, impaired bronchial patency, decreased cough reflex, etc. A special place in the pathogenesis of lung damage in pneumococcal infection is given to dysfunction of the ciliated epithelium of the bronchi, as well as changes in the chemical composition and rheological properties of bronchial secretions.
As a result of the interaction of micro- and macroorganisms in the bronchopulmonary system, a focus of inflammation is formed with a characteristic morphological substrate inherent in certain clinical forms of the disease (bronchitis, pneumonia, pleurisy, etc.).
From the primary lesion, pneumococci begin to spread with the flow of lymph and blood, forming prolonged bacteremia. Clinically, this can manifest itself as infectious-toxic syndrome, but asymptomatic bacteremia is also possible.
In weakened children, pneumococci can cross the blood-brain barrier and cause purulent meningitis or meningoencephalitis.
Spread of infection by contact bronchogenic route can lead to development of purulent pleurisy, sinusitis, otitis media, mastoiditis, pericarditis, epidural abscess, empyema. Pneumococcal bacteremia can result in development of osteomyelitis, purulent arthritis, brain abscess.
Severe forms of pneumococcal infection develop almost exclusively in young children, and the severity of clinical forms is determined not only by the reactivity of the macroorganism, but also by the virulence of the pathogen. The infection is especially severe with massive bacteremia and a high concentration of capsular antigen in the blood.
In severe cases, pneumococcal infection is accompanied by the development of rheological and hemodynamic disorders up to the occurrence of disseminated intravascular coagulation, acute adrenal insufficiency, edema and swelling of the brain tissue.