PULMONARY DEFENSE MECHANISMS
The respiratory tract is in constant contact with the environment and exposed to direct inoculation by infectious agents. Various defense mechanisms exist to prevent infections. Anatomic barriers represent the first line of defense. Large (>5 µm) airborne particles are trapped by the nasal cilia. Intermediate (1–5 µm) particles are deposited in the trachea and bronchi, and small (0.01–1 µm) particles are deposited in the bronchioles and alveolar spaces. The respiratory tract from the trachea to the bronchioles is lined with ciliary cells and with goblet cells that secrete a thin layer of mucus. The rhythmic beat of the cilia moves the mucus-trapped material upward, which is then cleared externally by the cough mechanism or swallowed interiorly and eliminated by the gastrointestinal tract. This mechanism is called the mucociliary escalator (Fig. 106-1).
Innate (nonspecific) immune mechanisms include the following:
Soluble proteins such as defensins, collectins, ficolins, pentraxins, surfactant proteins, and the complement system form the next line of defense. These proteins may destroy micro-organisms directly or indirectly by inducing opsonization, chemokine production, complement activation, and CD4+ T-cell proliferation.1
Innate cellular response: neutrophils, macrophages, and natural killer lymphocytes (NK cells) participate in the cellular response that can destroy the micro-organisms.
Dendritic cells are the major antigen-presenting cells and aid in the generation of adaptive immunity.
Adaptive immunity is the antigen-specific immune response. The response may be humoral (typically, IgA and IgG) or cell mediated.
Community-Acquired Pneumonia (CAP)
Staphylococcus pneumoniae and viruses are the most common pathogens identified.2 In the outpatient setting, CAP is most often treated empirically. Hospitalized patients with CAP should have sputum and blood cultures tested. Patients should also be tested for influenza during the influenza season. Methicillin-resistant Staphylococcus aureus (MRSA) has been identified in a small number of patients with CAP and should be considered, especially in patients with postinfluenza pneumonia, in those with risk factors for MRSA colonization, and in those with poor response to initial therapy.
This type of pneumonia can be caused by a wide variety of organisms. Commonly identified organisms include S. aureus, including MRSA, and gram-negative bacteria such as Pseudomonas aeruginosa.3
Principles of antibiotic therapy for pneumonia can be summed up as early, aggressive therapy and rapid de-escalation. Antibiotics should be started as soon as possible. Delay in antibiotic initiation has been associated with poorer outcomes.4 Recommended options for initial antibiotics have been published by various societies.5,6 Severity of the patient’s illness, medical comorbidities, and local antibiotic resistance patterns will influence the choice of initial antibiotics. Once the etiologic agent has been identified, antibiotics should be de-escalated ...