Pneumonia
Etiology and Pathogenesis
The host defenses of the lung are constantly challenged by a variety of organisms, including both viruses and bacteria (see Chapter 22). Viruses in particular are likely to avoid or overwhelm some of the upper respiratory tract defenses, causing a transient, relatively mild clinical illness with symptoms limited to the upper respiratory tract. When host defense mechanisms of the upper and lower respiratory tracts are overwhelmed, microorganisms may establish residence, proliferate, and cause a frank infectious process within the pulmonary parenchyma. With particularly virulent organisms, no major impairment of host defense mechanisms is needed; pneumonia may occur even in normal and otherwise healthy individuals. At the other extreme, if host defense mechanisms are quite impaired, microorganisms that are not particularly virulent and unlikely to cause disease in a healthy host may produce a life-threatening pneumonia.
In practice, several factors frequently cause enough impairment of host defenses to contribute to the development of pneumonia, even though individuals with such impairment are not considered “immunosuppressed.” Viral upper respiratory tract infections, ethanol abuse, cigarette smoking, heart failure, and preexisting chronic obstructive pulmonary disease (COPD) are a few of the contributing factors. More severe impairment of host defenses is caused by diseases associated with immunosuppression (e.g., advanced AIDS), various underlying malignancies (particularly leukemia and lymphoma), and use of corticosteroids and other immunosuppressive or cytotoxic drugs. In these cases associated with impairment of host defenses, individuals are susceptible to both bacterial and more unusual nonbacterial infections (see Chapters 24 to 26).
Bacteria
S. pneumoniae, a normal inhabitant of the oropharynx in a large proportion of adults, is a gram-positive coccus seen in pairs or diplococci. Pneumococcal pneumonia is commonly acquired in the community (i.e., in nonhospitalized patients) and frequently occurs following a viral upper respiratory tract infection. The organism has a polysaccharide capsule that interferes with phagocytosis and therefore is an important factor in its virulence. There are many antigenic types of capsular polysaccharide, and for host defense cells to phagocytize the organism, antibody against the particular capsular type must be present. Antibodies contributing in this way to the phagocytic process are called opsonins (see Chapter 22).
Many other types of bacteria can cause pneumonia. Because all of them cannot be covered in this chapter, the interested reader should consult some of the more detailed publications listed in the references at the end of this chapter.
Pathology
Lobar Pneumonia.Lobar pneumonia has classically been described as a process not limited to segmental boundaries but rather tending to spread throughout an entire lobe of the lung. Spread of the infection is believed to occur from alveolus to alveolus and from acinus to acinus through interalveolar pores known as the pores of Kohn. The classic example of a lobar pneumonia is that due to S. pneumoniae, although many cases of pneumonia documented as being due to pneumococcus do not necessarily follow this typical pattern.
Bronchopneumonia.In bronchopneumonia, distal airway inflammation is prominent along with alveolar disease, and spread of the infection and the inflammatory process tends to occur through airways rather than through adjacent alveoli and acini. Whereas lobar pneumonias appear as dense consolidations involving part or all of a lobe, bronchopneumonias are more patchy in distribution, depending on where spread by airways has occurred. Many bacteria, such as staphylococci and a variety of gram-negative bacilli, may produce this patchy pattern.
Interstitial Pneumonia.In some cases of pneumonia, the organisms are not highly destructive to lung tissue even though an exuberant inflammatory process may be seen. Pneumococcal pneumonia classically (although not always) behaves in this way, and the healing process is associated with restoration of relatively normal parenchymal architecture. In other cases, when the organisms are more destructive, tissue necrosis may occur, with resulting cavity formation or scarring of the parenchyma. Many cases of staphylococcal and anaerobic pneumonias follow this more destructive course.