How is pneumonia diagnosed?
How should the decision be made to hospitalize the patient?
What are the major infectious causes of community-acquired pneumonia?
What empiric antibiotic therapies are appropriate in community-acquired pneumonia?
What steps should be taken for patients not responding to usual therapy for community-acquired pneumonia?
Almost a million episodes of community-acquired pneumonia (CAP) occur each year in the United States in patients over the age of 65 years. While most clinicians are familiar with CAP, its diagnosis remains imprecise, its microbiology is often elusive, and management is usually empiric. Pneumonia is defined as a lung infection, characterized by cough, fever, and a pulmonary infiltrate, often with sputum production. If this sounds obvious, the reader is too easily deceived. Patients with pneumonia may not cough, a variable proportion have sputum, elderly patients are usually afebrile when first evaluated, and infiltrates may be hard to detect, especially in high-risk adults with chronic lung disease, the obese, or those for whom only a portable chest radiograph is available.
To complicate matters, many noninfectious illnesses are also characterized by cough, fever, and pulmonary infiltrates. Some of these are even called pneumonia, such as cryptogenic organizing pneumonia, sarcoid pneumonia, and lupus pneumonitis, and they may in every way mimic pneumonia as already defined. Taken together, all these infectious and noninfectious conditions cause what could be called a pneumonia syndrome. The more experienced recognizes the diverse etiologies of the pneumonia syndrome and should be unhappy about pigeonholing a patient under the rubric of CAP without considering other etiologies.
An array of host factors protects the lower respiratory tract against inhaled or aspirated organisms. The predisposition to pneumonia increases to the extent that these factors are altered or bypassed.
The configuration of the upper airways ensures that a thin, laminar flow of air passes close to hairs and sticky surfaces that can trap potentially infectious particles. Secretory immunoglobulin A (IgA), which constitutes 10% of the protein in nasal secretions, neutralizes viruses. These and other immunoglobulins appear to prevent bacterial colonization, probably by blocking binding sites on bacterial surfaces. Closure of the epiglottis prevents food particles from passing into the trachea during swallowing. The larynx prevents the passage of secretions into the trachea and allows the generation of intrapulmonic pressure needed for an effective cough. When particles bypass these mechanisms, ciliary action of epithelial cells moves them steadily upward toward the larynx; the cough reflex propels them more rapidly in the same direction. Tracheobronchial secretions maintain moist surfaces, and pulmonary surfactant probably helps to prevent atelectasis, which might interfere with clearance distally.
When infective agents bypass these mechanisms and reach the alveoli, several innate (nonspecific) and specific defenses come into play. Cells that line the respiratory tract produce substances that kill microorganisms or opsonize them for phagocytosis, including lysozyme, lactoferrin, beta-defensins, and surfactant. Bacterial cell wall components, such as lipopolysaccharide ...