Causes and pathogenesis of pneumococcal infection
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Causes of pneumococcal infection
According to the modern classification of pneumococci are referred to the family Streptococcaceae, the genus Streptococcus. These are Gram-positive cocci of an oval or spherical shape 0.5-1.25 μm in size, arranged in pairs, sometimes in the form of short chains. Pneumococci have a well-organized capsule. By its polysaccharide composition, more than 85 serotypes (serovars) of pneumococci have been isolated. Pathogens for humans are only smooth capsular strains, which, with the help of special serums, belong to one of the first 8 types, the remaining serovars for humans are weakly pathogenic.
When the pneumococcus is destroyed, endotoxin is released.
Pathogenesis of pneumococcal infection
Pneumococci can affect any organs and systems, but the triple organ should be considered lung and respiratory tract. The causes that determine the tropism of pneumococci to the bronchopulmonary system have not been established for certain. It is more likely that capsular pneumococcal antigens have an affinity for lung tissues and respiratory tract epithelium. The introduction of an agent into the lung tissue is promoted by acute respiratory diseases, 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 antigens elimination system are also important: defects in the lung surfactant system, inadequate phagocytic activity of neutrophils and alveolar macrophages, impaired bronchial patency, decreased cough reflex, etc. A special place in the pathogenesis of pulmonary disease in pneumococcal infection is attributed to dysfunction of the ciliary epithelium bronchi, as well as changes in the chemical composition and rheological properties of bronchial secretions.
As a result of the interaction of the micro- and macroorganism in the bronchopulmonary system, a focus of inflammation with a characteristic morphological substrate characteristic of one or another clinical form of the disease (bronchitis, pneumonia, pleurisy, etc.) is formed.
From the primary lesion, pneumococci begin to spread with a current of lymph and blood, forming a prolonged bacteremia. Clinically, this can manifest as an infectious-toxic syndrome, but asymptomatic bacteremia is also possible.
In weakened children, pneumococci can overcome the blood-brain barrier and cause purulent meningitis or meningoencephalitis.
The spread of infection by contact bronchogenic way can lead to purulent pleurisy, sinusitis, otitis media, mastoiditis, pericarditis, epidural abscess, empyema. Pneumococcal bacteremia can result in the development of osteomyelitis, purulent arthritis, and brain abscess.
Heavy forms of pneumococcal infection are formed almost exclusively in young children, while the severity of clinical forms is determined not only by the reactivity of the macroorganism, but also by the virulence of the pathogen. Especially severe infection occurs 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 until the occurrence of disseminated intravascular coagulation, acute adrenal insufficiency, swelling and swelling of brain material.
[