Respiratory mucosal cell destruction Viruses which cause pneumonia, such as influenza, infect and destroy ciliated epithelial cells. In addition to direct damage from infection itself or the resulting inflammatory reaction, viral infections may lead to prolonged airway dysfunction by causing small airway obstruction and hyperreactivity, predisposing to further infections. A small group of microorganisms seem to be adapted to survive in macrophages, so that containment or eradication may be difficult. Among these are pathogens that primarily or occasionally cause pneumonia, such as Mycobacterium tuberculosis and Legionella pneumophila. Alveolar macrophage inactivation Exfoliated epithelial cells infected by virus or viral droplets may reach the alveoli and infect macrophages, causing them to lose some of their bactericidal effectiveness.
Viral infections induce a variety of defects in alveolar macrophage bactericidal activity.
Although phagocytosis may be normal, intracellular killing is decreased in virally infected macrophages and subsequent bacterial infection and multiplication may occur. Streptococcus pneumoniae, group A streptococci, Hemophilus influenzae, Klebsiella pneumoniae, other Enterobacteriaceae, Staphylococcus aureus, anaerobes, Pseudomonas aeruginosa, Legionella pneumophila, Mycoplasma pneumoniae, influenzaviruses, Chlamydia, Pneumocystis carinii, and others. If invading organisms are able to establish infection, the lung parenchyma may mount an extensive inflammatory response leading to a clinical illness. Either direct generation of chemotactic factors by invading microorganisms, or chemotactic factors released by macrophages recruit secondary PMNs. The exuberant inflammatory response that often accompanies bacterial pneumonias is associated with purulent sputum and evidence of lung consolidation, a syndrome that has been referred to as typical pneumonia.