Acute Pneumonia

Roberto Barrios

Acute pneumonia is characterized by acute inflammation of the lung involving distal airspaces. Acute pneumonias can be classified in several different ways: according to epidemiology, pathogenesis, anatomic distribution, clinical presentation, and specific etiologic agent. The tissue response depends, to a certain extent, on the inflammatory response to specific etiologic agents. Streptococcus pneumoniae and Haemophilus influenzae often produce lobar consolidation, but tissue necrosis is rarely present. In contrast, staphylococci and many gram-negative bacilli often produce necrosis and even abscess formation. Classic examples of acute pneumonia, such as pneumococcal pneumonia, are characterized by abundant polymorphonuclear leukocyte exudates. In patients with lobar pneumonia, the lesions progress over time from edema to red hepatization, gray hepatization, and resolution. These classic descriptions are now rarely seen because of antibiotic administration, which has modified the natural history of the disease and has sharply reduced the overall case-fatality rate (Table 68.1).

Table 68.1. Major Causes of Infectious Pheumonia

Germ-positive cocci	Streptococcus pneumonia, Streptococcus pyogenes, other streptococci staphylococci
Gram-positive bacilli	Bacillus anthracis
Gram-negative cocci	Neisseria meningitidis, Moraxella catarrhalis
Gram-negative coccobacilli	Haemophilus influenzae; Gram-negatgive bacilli: Klebsiella pheumoniae, Pseudomonas sp., Escherichia coli, Proteus, Serratia sp., Acinetobacter, Yersinia pestis, Francisella tularensis, Enterobacter sp., Bacteroides, Legionella sp.
Mixed flora (frequently found in aspiration pneumonia)
Mycobacteria	Mycobacterium tuberculosis, Mycobacterium avium complex
Fungi	Hisoplasma, Coccidioides, Blastomyces, Cryptococcus, Candida, Aspergillus, Mucoraceae
Parasites	Pneumocystis carinii, Toxoplasma gondii
Mycoplasmas	Mycoplasma pneumoniae
Chlamydiae	Chlamydia psittaci, Chlamydia trachomatis, Chlamydia pneumoniae
Rickettsias	Coxiella brunetti
Viruses	Influenza virus, parainfluenza virus, adenovirus, respiratory syncytial virus, rhinovirus, measles virus, varicella zoster virus, cytomegalovirus
Modified from Simon HB, Pulmonary infections, In: Dale DC, ed, Scientific American Medicine, WebMD, 2003.

Histologic Features

Widespread fibrinopurulent consolidation of large areas.
Capillary congestion.
Acute (neutrophil-rich) inflammatory exudates filling alveoli and other distal airways.
Fibrin, edema, and debris admixed with inflammatory cells.
Occasional fibrin deposits within interalveolar pores.
Other changes (necrosis, vasculitis, abscess with cavitation) depend on other factors such as etiologic agent and host response.