Pneumonia is the most common cause of death from infectious diseases worldwide. Community-acquired pneumonia is believed to result, in most cases, from endogenous infection originating from oropharyngeal colonization. Bacteria such as Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pyogenes are found in the upper respiratory tracts of asymptomatic individuals.¹ In cases of S. aureus pneumonia, skin lesions are frequently present and are believed to be an additional source of endogenous pneumonia.

Inhalation of aerosolized respiratory or gastrointestinal secretions from infected persons is an uncommon route of infection for bacterial pneumonias. It is the most frequent method of spread for mycobacterial pneumonia (Chapter 40), mycoplasma pneumonia, and chlamydial (chlamydophila) pneumonia. Rarely, bacteria such as Yersinia pestis, Francisella tularensis, and Bacillus anthracis are causes of exogenous pneumonia. Legionella pneumophila is acquired by inhalation of infected water droplets from commercial sources such as cooling towers or air conditioning systems.

The most common symptom is cough, followed by sputum production, dyspnea, and chest pain. Chest x-ray typically shows an area of consolidation, with multilobar involvement in one-third of patients. An interstitial pattern is uncommon and associated with atypical pneumonia.

Complications occur in <25% of patients and include respiratory failure requiring mechanical ventilation, septic shock, and empyema.

The mortality of community-acquired pneumonia that requires hospitalization is 10%, and is higher in elderly patients and patients with comorbidities, bacteremia, and multidrug-resistant pathogens.²

The most common causes of community-acquired pneumonia requiring hospitalization are the “typical” bacteria: S. pneumoniae (the most common in all series), H. influenzae (usually the second most common), Serratia marcescens, S. aureus, Klebsiella pneumoniae, M. catarrhalis, enterobacteriaceae, and enterococci. In nonhospitalized patients, atypical bacteria (Mycoplasma pneumoniae and Chlamydophila pneumoniae) are the most common. Legionella pneumophila is a common cause in some series and usually occurs in outbreaks.³ The age at presentation is not associated with the infectious agent.²

Nosocomial pneumonia is defined as a pneumonia that is acquired by patients at least 2 to 3 days after being hospitalized. Most hospital-acquired pneumonias occur in patients on assisted ventilation (aka as ventilatorassociated pneumonia) who have been on prior antibiotics. The risk is proportional to the duration of mechanical ventilation with an overall risk of about 50%. There is a high mortality of between 40% and 50%.^6,7

The diagnosis is generally made clinically and based on new and persistent pulmonary opacities, purulent respiratory secretions, systemic signs of inflammatory response, and fever.⁸ Most occur within the first week after tracheotomy, with a median onset of 20 days after admission to the intensive care unit.⁸

The treatment is broad-spectrum antibiotics, which may be ineffectual due to the increase in multidrug-resistant organisms, especially Acinetobacter and Staphylococcus. Surgical intervention with pleural decortication may be required, if there is the development of abscesses with empyema.⁷

When patients are admitted to the hospital, there is a shift in the bacteria colonizing the upper respiratory tract, from predominantly Grampositive bacteria to Gram-negative bacteria.⁹ Tracheostomy performed for assisted breathing is associated with an increased risk for pneumonia, especially Gram-negative bacteria. Although tracheal aspirates show colonization with Gram-negative bacilli in the majority of hospitalized patients, preintubation tracheal cultures do not reliably predict the development of pneumonia.⁸

The specific agent is often not identified. The most frequent isolates in ventilator-associated pneumonia are Acinetobacter baumannii, Pseudomonas aeruginosa, Escherichia coli, S. aureus, Proteus mirabilis, K. pneumoniae, and H. influenzae.^6,8,10,11

Bacterial infections are the most frequent cause of pneumonia in transplant patients. Viral infections and pneumocystis pneumonia are also common and are usually treated prophylactically, especially early after transplantation (Chapters 39 and 42).

Pneumonia in transplant patients, similar to immunocompetent patients, may be community acquired or nosocomial. In solid organ transplants, the rate is ˜10 episodes of pneumonia per 1,000 recipients/year. A specific diagnosis is made in about two-thirds of patients. Bacterial causes are by far the most frequent and show a high rate of multidrug resistance when hospital acquired. Graft rejection or dysfunction occurs in about 20% of patients.¹⁵

Bacteria that result in transplant-related pneumonia include S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus, Nocardia, Mycobacterium tuberculosis, C. pneumoniae, and Veillonella species. In hospital-acquired multidrug-resistant cases, the most frequent organisms are P. aeruginosa, Enterobacteriaceae, S. aureus, A. baumannii, Stenotrophomonas maltophilia, and Burkholderia cepacia.^15,16

Neutropenia is the most important risk factor for pneumonia in patients with hematologic and solid malignancies. Neutrophils are sensitive to alkylating agents and nucleoside analogues and neutropenia is defined as severe when blood counts are below 500/mL.¹⁷

Infections are the leading cause for nonrelapse mortality in cancer patients. Despite early empirical antibiotic therapy, infection-related mortality in neutropenic cancer patients is 4% to 7%.¹⁸

The bacterial causes of pneumonias in cancer patients include common respiratory pathogens such as S. pneumoniae, S. aureus, and H. influenza as well as Gram-negative enteric organisms, including Pseudomonas spp., K. pneumoniae, E. coli, Enterobacter cloacae, S. maltophilia, Citrobacter spp., S. marcescens, A. baumannii-complex, and Proteus spp.^18,19,20

Typical pneumococcal pneumonia presents as a lobar consolidation, although focal consolidation also occurs. The inflammatory infiltrate consists of a mixture of polymorphonuclear neutrophils and macrophages. In the early stages of the infection, organisms are present in the infiltrate, and fibrin strands and leukocytes are intact. Most treated pneumococcal pneumonia resolve without sequelae, but cavitary disease may occur.

Historically, a specific diagnosis of S. pneumoniae can be made by applying polyvalent antiserum to capsular polysaccharide on sputum smears or tissue implants (the Quellung reaction). This procedure also works for other encapsulated bacteria such as K. pneumoniae.

S. pyogenes is a rare cause of community-acquired pneumonia.⁴ Abscess formation and empyema, sometimes with bronchopleural fistula formation, are more commonly seen than in pneumonias caused by S. pneumoniae.

Classified variously (sometimes as Streptococcus milleri), α-hemolytic streptococci may occasionally result in pneumonias and lung abscesses. They are frequently isolated from patients with empyema.²¹ The inhospital mortality rate for patients with empyema is 4% to 15%.²¹ Approximately 40% of patients require surgical intervention, in the form of pleural decortication.

Pneumonia can rarely occur in patients with sepsis secondary to N. meningitides, resulting in abscesses and empyema.^22,23

Historically, S. aureus pneumonia was recognized as a complication of influenza outbreaks. Currently, it is an uncommon cause of community-acquired pneumonia.^4,24 Staphylococcus aureus is emerging as a relatively common cause of nosocomial pneumonia, being the most common Gram-positive nosocomial pathogen, but less frequent than Gram-negative pneumonia.²⁵

Occasional necrotizing community-acquired pneumonias have been reported with methicillin-resistant S. aureus, often associated with skin lesions.²⁶ High virulence is associated with the formation of toxins such as Panton-Valentine leukocidin that cause extensive tissue necrosis. Strains forming this toxin are becoming more frequently resistant to methicillin and are associated with a high mortality.^27,28

Infections with S. aureus can result in a chronic granulomatous inflammatory response around clusters of organisms resembling sulfur granules of actinomycosis, which typically involve the skin. Rarely, viscera including the lung are involved.²⁹ Other bacteria can cause botryomycosis, primarily Gram-negative rods.