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Causes and pathogenesis of pleuropneumonia

, medical expert
Last reviewed: 23.04.2024
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Lobar bacterial pneumonia, or focal non-segmental pneumonia, or acute lobar inflammation of the lung lobes affecting part of its serous membrane (pleura) can be diagnosed as pleuropneumonia, although this definition is absent in the respiratory system class ICD-10.

Obviously, this is due to the fact that pleurisy — dry or  pleural effusion  — is most often seen as a consequence, that is, a complication of strepto-and staphylococcal pneumonia, which occurs, although not always, but in at least three to four cases of ten.

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Cause

Inflammation of the lungs is provoked by infection, and the most common cause of the development of pleuropneumonia (lobar pneumonia) has always been considered and today is considered to be Streptococcus pneumoniae pneumococcus - α-hemolytic streptococcus, anaerobic (which is part of the nasopharyngeal microbiota in healthy people).

Clinical studies have identified other causes of pleuropneumonia, and these are pathogens such as:

  • gamma-proteobacterium Klebsiella pneumoniae (Friedlander wand);
  • encapsulated and non-encapsulated strains of Haemophilus influenzae (Pfeiffer sticks) - commensal bacteria of the upper respiratory tract;
  • MRSA - methicillin-resistant Staphylococcus aureus (Staphylococcus aureus), causing pulmonary pleural form of  Staphylococcus pneumonia ;
  • Streptococcus pyogenes present in the pharyngeal mucosa is β-hemolytic streptococcus group A;
  • Pseudomonas aeruginosa (Asean purulent bacillus), provoking nosocomial (intra-hospital) pneumonia;

Among the more rare infections, pulmonologists name aquatic non-spore-forming Gram-negative bacilli Legionella pneumophila, which inhalation can cause severe pneumonia (with a fatality rate of up to 7-8%), as well as Mycoplasma pneumonia. The bacterium M. Pneumoniae, spread by airborne droplets and by contact, usually causes a lung infection of the respiratory system, and the most common disease is tracheobronchitis. However, as practice shows, in pediatric patients, M. Pneumoniae plays a certain role in the development of community-acquired pneumonia (up to 56-59% of cases among children four to six years old).

Pleuropneumonia can be the result of extensive parasitic invasions, in particular,  ascariasis in children. See also -  Causes of acute pneumonia in children.

Risk factors

Predisposing factors for the development of pleuropneumonia are the same as for any pneumonia, and among them are:

  • asymptomatic bacteriocarrier, in particular Streptococcus pneumoniae pneumococci (recorded in different parts of the world at levels from 13% to 87%);
  • infectious and inflammatory  complications of influenza ;
  • chronic diseases of the upper and lower respiratory tract, in particular, acute respiratory infections, tracheitis and bronchitis;
  • smoking and alcohol addiction;
  • temporary decrease in immunity and persistent immunodeficiency states;
  • prolonged adherence to bed rest (or forced lying position under certain conditions), leading to a deterioration in the ventilation of the lungs;
  • hereditary and autoimmune fibrosis associated with systemic scleroderma, lupus erythematosus, cystic fibrosis.

And the risk factors of hospital pneumonia are in the use of inhalation anesthesia (for surgical interventions), tracheal intubation and artificial respiration.

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Pathogenesis

As is known, the structural elements of the  lungs  are lobes consisting of segments, the tissue of which is lobules (lobules). The pulmonary lobes on the outside are surrounded by a thin connective tissue (serous) membrane - the visceral pleura, which also comes in between the lobes of the slit. A pleural fluid (usually 10–20 ml) is contained in the pleural cavity (formed by the leaves of the pleura, both parenteral and visceral), which facilitates movement between the lungs and the chest wall.

The lower airways are not sterile: they are always exposed to pathogens. The pathogenesis of inflammation caused by them is associated with the invasion and spread of the aforementioned bacteria in the lung parenchyma at the alveolar level, and the response to this invasion of the body's immune cells.

Alveolar macrophages of the lung tissue must absorb and destroy pathogens, but bacteria are able to overcome this defense and begin to multiply.

For example, pneumococcal toxin pneumolysin is an enzyme that is released from microbes and binds to the cholesterol of the cytoplasmic membrane of lung tissue cells to form pores — large oligomeric arc and ring structures that damage the cell membrane (so that the contents of the cell become available to the bacterium). The inflammatory response develops due to the binding of the toxin to the TLR4 receptors, and the proapoptotic effects result from the stimulation of the activity of inflammatory mediators, such as TNF-α, IL-1β, IL-8, G-CSF and prostaglandins.

And the impact of Legionella pneumophila bacteria is focused on the apoptosis of alveolar macrophages in the acini and respiratory bronchioles of the human lung.

In the case of pleuropneumonia, inflammation is accompanied by the appearance of an exudate containing fibrin and subsequent infiltration of individual sections or the entire tissue of the affected lung lobe, which leads to its structural changes - homogeneous compaction.

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Epidemiology

While in the United States and Canada, the frequency of pneumonia is more than 5 million cases per year, 80% of new cases are treated as outpatients, and lobar bacterial pneumonia or pleuropneumonia is diagnosed in 12 patients per thousand, and most often it is men. The risk of death in complex cases, CDC statistics estimated at 7.3% -11.6% (in Latin America -13.4%).

According to the European Respiratory Journal, up to 12.5% of cases of intrahospital pneumonia are caused by Staphylococcus aureus: the adult population usually ranges from 5.15 to 7.06 cases per thousand people per year, but at the age of less than 4 years and over 60 years - more 12 cases per thousand. The mortality rate for Europe is 9%.

trusted-source[13], [14], [15], [16], [17]

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