What is the pathology of pneumonia?

From the Guidelines

Pneumonia is characterized by inflammation of the lung parenchyma, typically caused by infectious agents including bacteria, viruses, fungi, or parasites, leading to consolidation of lung tissue and reduced gas exchange capacity. The pathology begins when pathogens enter the lower respiratory tract, triggering an inflammatory response. This response causes alveolar spaces to fill with exudate containing neutrophils, red blood cells, and fibrin. Microscopically, the alveoli show inflammatory infiltrates, edema, and sometimes microorganisms. Different pathogens create distinct pathological patterns: bacterial pneumonia often causes lobar consolidation with neutrophilic infiltration, while viral pneumonia typically presents with interstitial inflammation and lymphocytic infiltrates. The body's immune response, while necessary to combat infection, contributes significantly to tissue damage through the release of inflammatory mediators and proteolytic enzymes. Complications may include pleural effusion, empyema, lung abscess, or respiratory failure in severe cases. The pathological changes usually resolve completely with appropriate treatment, though some patients may develop fibrosis or other permanent lung changes, particularly in cases of severe or recurrent pneumonia, as noted in guidelines for managing community-acquired pneumonia 1.

Key aspects of pneumonia pathology include:

• Inflammation of the lung parenchyma
• Consolidation of lung tissue
• Reduced gas exchange capacity
• Inflammatory infiltrates and edema in the alveoli
• Potential for complications such as pleural effusion or respiratory failure
• Variability in pathological patterns based on the causative pathogen, with bacterial pneumonia often causing lobar consolidation and viral pneumonia presenting with interstitial inflammation, as discussed in the context of community-acquired pneumonia management 1.

The management of pneumonia involves determining the likely etiologic pathogens and selecting appropriate antimicrobial therapy, taking into account factors such as the presence of cardiopulmonary disease, risk factors for drug-resistant pneumococci, and the severity of illness at presentation, as outlined in guidelines for the management of adults with community-acquired pneumonia 1.

From the Research

Pathology of Pneumonia

The pathology of pneumonia is complex and involves various mechanisms, including inflammation and immune response.

• Pneumonia is an important cause of morbidity and mortality, and it is an unusual outcome of respiratory infection, as most of the time, microbes in the lung can be controlled by a combination of constitutive and recruited defense mechanisms 2.
• Inflammation is a key component of recruited defenses, and variations in inflammation can influence pneumonia susceptibility and severity 2.
• Pneumonia can be caused by a wide range of microorganisms, including bacteria, respiratory viruses, and fungi, and there are great geographical variations in their prevalence 3.
• The development of the disease largely depends on the host immune response, with pathogen characteristics having a less prominent role 3.

Types of Pneumonia

• Pneumonia can be broadly divided into community-acquired pneumonia or hospital-acquired pneumonia 3.
• Community-Acquired Pneumonia (CAP) is a major public health problem, and it has been estimated that 2,000 people are affected by CAP every year in Brazil alone 4.
• Secondary bacterial pneumonia is an important cause of influenza-associated death, and antiviral therapy has been shown to improve survival in mice with secondary pneumococcal pneumonia after influenza 5.

Histopathology of Pneumonia

• Murine acute lung infection models mirror human pathologies in many aspects and contribute to our understanding of the disease and the development of novel treatment strategies 6.
• The histopathological features of established models of acute pneumonia in mice induced by different pathogens, such as Streptococcus pneumoniae, Staphylococcus aureus, and influenza A virus, have been systematically described and compared 6.
• Systematic comparisons of the models revealed striking differences in the distribution of lesions, the characteristics of pneumonia induced, principal inflammatory cell types, lesions in adjacent tissues, and the detectability of the pathogens in histological sections 6.