Main routes of infection entry
Microorganisms penetrate the lung tissues via four main pathways:
- Airborne — with inhaled air.
- Aspiration — from the naso- and oropharynx.
- Hematogenous — from infection foci located in other parts of the body.
- Contact — via the spread of inflammation from adjacent affected areas.
Airborne and aspiration pathways are of the greatest importance in the development of inflammation, especially when the natural defense barriers of the lungs are compromised.
Classification by pathogenesis
In domestic medical practice, E.V. Gembitskaya's classification is widely used. Based on the mechanism of onset, two large groups are distinguished:
- Primary pneumonias act as independent diseases and develop in individuals without prior pulmonary pathology (e.g., lobar form or Legionnaires' disease).
- Secondary pneumonias occur much more frequently. They accompany somatic diseases, chronic respiratory pathologies, or infections with a primary focus outside the lungs. This also includes absolutely all hospital-acquired variants.
Nosocomial (hospital-acquired) pneumonias
Such pathologies are recorded later than 48 hours after the patient's admission to the hospital. The overall share among all hospitalized patients is 8.5%, in intensive care units this figure rises to 13%, and in tumor chemotherapy departments it reaches 30%.
The main causative agents of hospital-acquired infections are most often gram-negative aerobic bacteria, including Klebsiella, Pseudomonas aeruginosa, Escherichia coli, Proteus, as well as staphylococci and streptococci. The disease is often characterized by mixed flora.
Interstitial inflammation and process forms
In interstitial inflammation, the inflammatory process involves the alveolar wall and interstitial tissue of the respiratory divisions, while secondary accumulation of exudate occurs in the alveolar lumens. Such conditions are often referred to as acute pneumonitis or atypical pneumonia.
The clinical-morphological classification distinguishes three main forms:
- Lobar (croupous)
- Bronchopneumonia (focal)
- Acute interstitial (acute pneumonitis)
Briefly: answers to topical questions
What stages of pathogenesis are distinguished in lobar pneumonia?
In lobar pneumonia, four classical pathomorphological stages are distinguished.
- Stage of engorgement — rapid filling of the alveoli with fibrinous exudate containing pneumococci.
- Stage of red hepatization (consolidation) — erythrocytes predominate in the exudate with a small admixture of neutrophils.
- Stage of gray hepatization (consolidation) — mass appearance of leukocytes (neutrophils) carrying out bacterial phagocytosis.
- Stage of resolution — resorption of the exudate and restoration of the lung tissue structure (sometimes this stage is combined with convalescence).
What pulmonary complications are characteristic of lobar pneumonia?
Pulmonary complications of lobar pneumonia include processes of destruction and impaired organization of the exudate.
- Carnification — organization of unresorbed fibrinous exudate by connective tissue resulting in lobar pneumosclerosis.
- Lung abscess — occurs with excessive neutrophil activity and the addition of secondary pyogenic flora.
- Lung gangrene — develops when putrefactive microflora joins.
- Pleural empyema — suppurative fusion of fibrinous pleural deposits.
Exudative pleurisy and acute respiratory failure are also considered pulmonary complications.
What extrapulmonary complications can develop in lobar pneumonia?
Extrapulmonary complications of lobar pneumonia are associated with lymphogenous or hematogenous generalization of the infection.
- Lymphogenous — purulent mediastinitis and purulent pericarditis.
- Hematogenous — metastatic brain abscesses, purulent meningitis, acute ulcerative or polypoid-ulcerative endocarditis (more often of the tricuspid valve), purulent arthritis, peritonitis, and sepsis.
Bacteremia in lobar pneumonia is registered in 30% of cases.
What microscopic changes are observed in the alveoli during the stage of gray hepatization?
During the stage of gray hepatization, microscopic examination of the alveoli reveals an accumulation of specific inflammatory exudate and changes in capillaries.
- Vascular changes — collapse of pulmonary capillaries is noted.
- Exudate composition — the alveoli are entirely filled with fibrinous exudate containing a high concentration of living and dead polymorphonuclear leukocytes (neutrophils) and macrophages.
- Cellular functions — massively appeared granulocytes perform phagocytosis of opsonized pneumococci and fibrin lysis, while macrophages phagocytose necrotic detritus.
Which diseases and conditions are most often complicated by secondary pneumonia?
Secondary pneumonias develop against the background of various pathological processes and body conditions. Most often they complicate:
- Chronic bronchopulmonary diseases.
- Various somatic diseases.
- Other infections where the primary affect is located outside the lungs (for example, severe forms of influenza are often complicated by secondary bacterial pneumonia).
Also, all cases of nosocomial (hospital-acquired) acute pneumonias belong to secondary ones.
The four pathways of infection entry (Airborne, Aspiration, Hematogenous, Contact) can be remembered using the mnemonic device.
Class and exam questions
What are the main causative agents typical of nosocomial pneumonia?
Hospital-acquired infections are usually caused by gram-negative aerobic bacteria with mixed flora. These include Klebsiella, Pseudomonas aeruginosa, Escherichia coli, Proteus, staphylococci, and streptococci.
What is the difference between primary and secondary pneumonia?
Primary pneumonias occur as independent diseases in healthy individuals. Secondary ones develop against the background of chronic bronchial pathology, somatic diseases, or other infections.
What is interstitial inflammation of the lungs and what is its alternative name?
This is inflammation affecting the alveolar wall and interstitial tissue with secondary accumulation of exudate in the alveoli. Synonyms for this condition are acute pneumonitis and atypical pneumonia.
What else to study on this topic
- Etiological features and mechanisms of damage to the pulmonary parenchyma by viruses and pyogenic bacteria
- Risk factors for the development of acute pneumonia, including smoking, immunodeficiencies, and airway obstruction
- Classification of bronchopneumonia by the extent of the process
- Timeline and division of nosocomial pneumonia by the time of onset in the hospital
- Statistical indicators of morbidity and mortality in the Russian Federation and the USA
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