The student will be able to describe the three main inflammatory responses to pulmonary infection (intra-alveolar suppurative, interstitial mononuclear, and granulomatous) and identify characteristic microbiological etiologies for each.
The student will be able to distinguish bronchopneumonia from lobar pneumonia and identify specific etiologies of each.
The student will be able to describe the clinical settings in which a lung abscess can develop and identify microorganisms that can cause abscess formation.
The student will be able to distinguish primary tuberculosis from secondary (reactivation) tuberculosis, based on morphologic as well as clinical features.
The student will be able to recognize common fungi causing pulmonary infection.
The student will be able to describe Pneumocystis jiroveci pneumonia and recognize the causative microorganism.
As summarized in Chap. 10, the respiratory system has many defenses against infectious disease. The vibrissae in the nose and the mucociliary covering of the mucosa in the conducting portion of the respiratory system trap particles and micro-organisms, moving them cephalad to the pharynx to be expectorated or swallowed. Macrophages within the respiratory parenchyma phagocytize small particles and microorganisms and, if overwhelmed, recruit neutrophils from alveolar septal capillaries. Finally, immunoglobulin A in the mucosal secretions supports humoral immunity. In general, suboptimal humoral immunity and/or suboptimal nonimmune defense systems increase the risk for pyogenic bacterial infection, whereas suboptimal cell-mediated immunity increases the risk of infection by intracellular and low-virulence organisms, typically viruses and some bacteria. Other risk factors for the development of respiratory tract infection include decreased/absent cough reflex, reduced phagocytic/bactericidal activity of alveolar macrophages (eg, by alcohol, smoking, anoxia, oxygen intoxication), pulmonary congestion/edema, accumulation of airway secretions (eg, cystic fibrosis or distal to an obstruction), and mucociliary dysfunction, both congenital (eg, immotile cilia syndrome, Kartagener syndrome) and acquired (eg, viral illness, toxic effects of inhaled smoke).
This chapter will focus on the pathology of infectious disease and is organized by general morphologic similarities. There are three major morphologic patterns in infections of the respiratory tract: intra-alveolar accumulation of neutrophils, with or without abscess formation; interstitial expansion by mononuclear inflammatory cells; and granulomatous inflammation. Lung infections can also be organized based on their clinical settings rather than by their morphologic patterns (Table 34.1).
Table 34.1The pneumonia syndromes organized by clinical setting |Favorite Table|Download (.pdf) Table 34.1 The pneumonia syndromes organized by clinical setting
|Community-Acquired Acute Pneumonia ||Community-Acquired Atypical Pneumonias |
|Streptococcus pneumoniae ||Mycoplasma pneumoniae |
|Haemophilus influenzae ||Chlamydia spp. |
|Moraxella catarrhalis ||Coxiella burnetii (Q fever) |
|Staphylococcus aureus ||Respiratory syncytial virus |
|Legionella pneumophila ||Parainfluenza virus (children) |
|Klebsiella pneumoniae ||Influenza A & B viruses (adults) |
|Pseudomonas spp. ||Adenovirus, SARS virus |
|Hospital-Acquired Pneumonia ||Aspiration Pneumonia (usually mixed flora) |
|Klebsiella spp. ||Bacteroides spp. ||Prevotella spp. |
|Serratia marcescens ||Fusobacterium spp. ||S. pneumoniae |
|Escherichia coli ||Peptostreptococcus spp. |
|S. aureus ||S. aureus ||H. influenzae |
|Pseudomonas spp. ||Pseudomonas aeruginosa |
|Chronic Pneumonia ||Necrotizing Pneumonia and Lung Abscess |
|Nocardia asteroides ||Anaerobic ...|