eMedicine Specialties > Pulmonology > Infectious Lung Diseases
Pneumonia, Bacterial
Updated: Aug 21, 2009
Introduction
Background
Definition
Pneumonia can be generally defined as inflammation of the lung parenchyma; pneumonia is characterized by consolidation of the affected part and a filling of the alveolar air spaces with exudate, inflammatory cells, and fibrin. Most cases of pneumonia are due to infection by bacteria or viruses, although they may also be due to the inhalation of chemicals, trauma to the chest wall, or other infectious agents such as rickettsiae, fungi, and yeasts.1
Classification and categorization of bacterial pneumonia
Discussion of bacterial pneumonia involves classification and categorization schemes based on various characteristics of the illness, such as anatomic or radiologic distribution, the setting or mechanism of acquisition, and the pathogen responsible.
- Anatomic/radiographic patterns of pneumonia2,3
- Lobar pneumonia: Lobar pneumonia is also known as focal or nonsegmental pneumonia. Radiographically, lobar pneumonia is manifested as nonsegmental, homogenous consolidation involving one, or less commonly, multiple lobes. Larger bronchi often remain patent with air, creating the characteristic air bronchogram. Lobar consolidation is pathologically the result of the rapid production of edema fluid with minimal cellular reaction, occurring initially in the lung periphery and then spreading between acini through the pores of Kohn and canals of Lambert.
- Bronchopneumonia: Also known as multifocal or lobular pneumonia, bronchopneumonia is radiographically identified by its patchy appearance, with peribronchial thickening and poorly defined air-space opacities. As illness becomes more severe, consolidation involving the terminal and respiratory bronchioles and alveoli results in the development of centrilobular nodular opacities or air-space nodules; this consolidation can develop further and coalesce to give a lobular or lobar pattern of involvement. Typically, air bronchograms are absent. The pathogens known to cause this pattern of pneumonia are particularly destructive; thus, abscesses, pneumatoceles, and pulmonary gangrene are often seen. Pathologically, bronchopneumonia stems from inflammation of large airways (bronchitis) with patchy (lobular) involvement.
- Interstitial pneumonia: Interstitial pneumonia may be further classified as focal or diffuse. Pathologically, the radiographic pattern results from edema and inflammatory cellular infiltrate into the interstitial tissue of the lung. The pathologic development of interstitial pneumonia generally takes 1 of 2 forms: (1) an insidious infectious course that results in lymphatic infiltration of alveolar septa without parenchymal abnormality or (2) acute or rapidly progressive disease that results in diffuse alveolar damage affecting the interstitial and air spaces. Radiographically, the disease manifests with a reticular or reticulonodular pattern.
- Setting of infection - The alphabet soup of pneumonia: A major part of what distinguishes these various categories from each other is the varying risk of exposure to multidrug-resistant (MDR) organisms.4,5,6
- Community-acquired pneumonia: Defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital, community-acquired pneumonia (CAP) should not meet the criteria for health care–associated pneumonia (HCAP), as defined below.
- Health care–associated pneumonia and nursing home–associated pneumonia:HCAP is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital in patients with increased risk of exposure to MDR bacteria as a cause of infection. Risk factors for exposure to MDR bacteria in HCAP include the following:
- Hospitalization for 2 or more days in an acute care facility within 90 days of current illness
- Exposure to antibiotics, chemotherapy, or wound care within 30 days of current illness
- Residence in a nursing home or long-term care facility
- Hemodialysis at a hospital or clinic
- Home nursing care (infusion therapy, wound care)
- Contact with a family member or other close person with infection due to MDR bacteria
- NHAP is generally included in the category of HCAP because of the high incidence of infection with gram-negative bacilli and Staphylococcus aureus. However, some authors accept NHAP as a separate entity because of distinct epidemiological associations with infection in nonhospital health care settings.1 Importantly note that nursing home patients with pneumonia are less likely to present with the classic signs and symptoms of the typical pneumonia presentation, such as fever, chills, chest pain, and productive cough, but instead often have delirium and altered mental status. Pneumonia in patients in nursing homes and long-term care facilities has been associated with greater mortality than in patients with CAP. These differences may be due to factors such as disparities in functional status, likelihood of exposure to infectious agents, and variations in pathogen virulence, among others. Thus, the degree to which the HCAP definition applies to such settings is not yetclear.4,5
- Hospital-acquired pneumonia:Hospital-acquired pneumonia (HAP) is defined as pneumonia that develops at least 48 hours after admission to a hospital. Risk factors for exposure to MDR organisms in HAP include the following:
- Antibiotic therapy within 90 days of the hospital-acquired infection
- Current length of hospitalization of 5 days or more
- High frequency of antibiotic resistance in the local community or within the specific hospital unit
- Immunosuppressive disease or therapy
- Presence of HCAP risk factors for exposure to MDR bacteria
- Ventilator-associated pneumonia: Ventilator-associated pneumonia (VAP) is defined as pneumonia that develops more than 48 hours after endotracheal intubation or within 48 hours of extubation. Risk factors for exposure to MDR bacteria causing VAP are the same as those for HCAP and/or HAP.4,6
- A note on nosocomial pneumonia: Nosocomial infections are generally described as those acquired in the hospital setting. The term nosocomial pneumonia has evolved into the more succinct clinical entities of HAP and VAP; however, the term nosocomial pneumonia still has an appropriate place in the descriptive language of pneumonia. Nosocomial infections have been viewed as a "tribute to pay to the more aggressive management of the population, characterized by the use of sophisticated technologies and invasive devices," an important consideration in the pulmonary care of critically ill patients.7
Aspiration pneumonia
Aspiration pneumonia develops after the inhalation of oropharyngeal secretions and colonized organisms. While organisms frequently implicated in CAP, such as Haemophilus influenzae and Streptococcus pneumoniae, can colonize the nasopharynx and oropharynx and their aspiration can contribute to the development of CAP, the term aspiration pneumonia refers specifically to the development of an infectious infiltrate in patients who are at increased risk of oropharyngeal aspiration.Patients may be at increased risk of aspiration and/or the development of aspiration pneumonia for a number of reasons, as follows:
- Decreased ability to clear oropharyngeal secretions - Poor cough or gag reflex, impaired swallowing mechanism (eg, dysphagia in stroke patients), impaired ciliary transport (eg, from smoking)
- Increased volume of secretions
- Increased bacterial burden of secretions
- Presence of other comorbidities - Anatomic abnormalities, gastroesophageal reflux disease (GERD), achalasia
- The challenge of appropriate, risk-minimizing positioning
- Gastroparesis/dysmotility
- Impaired cough/gag/swallow reflexes (illness- or drug-induced)
- Impaired immune response
- Intubation/extubation
Historically, the bacteria implicated in aspiration pneumonia have been the anaerobic oropharyngeal colonizers such as Peptostreptococcus, Bacteroides, Fusobacterium, and Prevotella species However, now evident is that the vast majority of cases of aspiration pneumonia result from the same pathogens implicated in CAP and HAP, depending on the setting in which the aspiration event occurred. The clinical course of aspiration pneumonia is, thus, similar to that of CAP or HAP.8
Pathophysiology
Bacterial pathogens of pneumonia and some notable features
Although pneumonia may be caused by myriad pathogens, a limited number of agents are responsible for most cases; these common agents marked below with an asterisk.9,10,11,12
- Atypical organisms: As previously mentioned, atypical organisms are generally associated with a milder form of pneumonia. Another feature that often makes these organisms atypical is the inability to detect them on Gram stain or to cultivate them in standard bacteriologic media.9,10
- Mycoplasma pneumonia: Mycoplasmas are the smallest known free-living organisms in existence; they lack cell walls (and therefore are not apparent after Gram stain) but do have protective 3-layered cell membranes.
- Chlamydophila species (Chlamydophila psittaci, Chlamydophila pneumoniae): Psittacosis, also known as parrot disease or parrot fever, is caused by C psittaci and is associated with the handling of various types of birds.
- Legionella species: Legionella species are gram-negative bacteria found in freshwater; they are known to grow in complex water distribution systems. (Institutional water contamination is frequently noted in endemic outbreaks.) Legionella species are the causative agent of Legionnaires disease. Patients often present with mental status changes or diarrhea. Patients may develop hemoptysis or pulmonary cavitations. Hyponatremia is often noted in correlation with Legionella infection.
- Coxiella burnetii: C burnetii is the causative agent of Q fever. It is spread from animals to humans; person-to-person transmission is unusual. Animal reservoirs typically include cats, sheep, and cattle.
- Bordetella pertussis: B pertussis is the agent responsible for pertussis or whooping cough. Pertussis is often characterized by its long course of symptomatic cough in adults and by the presence of a whooping sound and/or posttussive vomiting in children.
- Typical organisms: While several of these organisms are the usual causes of the typical presentation of pneumonia (again marked with an asterisk), many of them are much less common causes of pulmonary infection.
- Gram-positive bacteria
- S pneumoniae: A facultative anaerobe identified by its chainlike staining pattern. Presentation of pneumococcus is classically associated with a cough productive of rust-colored sputum.
- S aureus: S aureus is a facultative anaerobe identified by its clusterlike staining pattern. Methicillin-resistant S aureus (MRSA) has had a large impact on empiric antibiotic choices at many institutions.
- Enterococcus (Enterococcus faecalis, Enterococcus faecium): These organisms are group D streptococci that are well-known normal gut florae. They can be identified by their pair-and-chain staining pattern. The emergence of vancomycin-resistant Enterococcus (VRE) is indicative of the importance of appropriate antibiotic use.
- Actinomyces israelii: This is a beaded, filamentous anaerobic organism that grows as normal flora in the GI tract. A israelii is known to form abscess and sulfur granules.
- Nocardia asteroides: N asteroides is a weakly gram-positive, partially acid-fast bacillus that forms partially acid-fast beaded branching thing filaments. It is known to cause lung abscesses and cavitations. Erosion into the pleura can also occur, resulting in hematologic spread of the organism.
- Gram-negative bacteria
- Pseudomonas aeruginosa: P aeruginosa is an aerobic, motile bacillus often characterized by its distinct (grapelike) odor.
- Klebsiella pneumoniae: K pneumoniae is a facultatively anaerobic, encapsulated bacillus. Presentation of Klebsiella pneumonia is classically associated with a cough productive of red currant-jelly sputum.
- Haemophilus influenzae: H influenzae is an aerobic bacillus that may be encapsulated. Several major subtypes have been identified, which have varying levels of pathogenicity; encapsulated type b is known to be a major factor in virulence, although routine vaccination against this particular subtype has decreased the prevalence of severe disease caused by H influenzae.
- Escherichia coli: E coli is a facultatively anaerobic, motile bacillus; it is well known to colonize the lower GI tract and produce the essential vitamin K.
- Moraxella catarrhalis: M catarrhalis is an aerobic diplococcus known as a common colonizer of the respiratory tract.
- Acinetobacter baumannii: A baumannii is a pathogen that has been well described in the context of VAP.
- Francisella tularensis: F tularensis is the causative agent of tularemia, or rabbit fever. F tularensis is a facultative intracellular bacterium that multiplies within macrophages. It is typically transmitted to humans via a tick bite; its reservoir animals include rodents, rabbits, and hares. F tularensis can also be transmitted in an airborne manner or contracted from handling dead, infected animals. It is commonly spoken of in terms of its potential use as a biological weapon.13
- Bacillus anthracis: B anthracis is the agent responsible for inhalational anthrax.
- Yersinia pestis: Y pestis infection is better known as the plague.
- Gram-positive bacteria
- Anaerobic organisms associated with aspiration pneumonia: Pneumonia due to anaerobes typically results from aspiration of oropharyngeal contents, as previously mentioned. These infections tend to be polymicrobial and may consist of the following anaerobic species, some of which have already been discussed above: Klebsiella, Peptostreptococcus, Bacteroides, Fusobacterium, and Prevotella.
- Additional bacteriologic pulmonary pathogens, such as the Mycobacteria, may be discussed elsewhere in the eMedicine journal.
Pathology of pneumonia
- The pneumonic inflammatory process
- During pulmonary infection, acute inflammation results in the migration of neutrophils out of capillaries and into the air spaces, forming a marginated pool of neutrophils that is ready to respond when needed. They phagocytize microbes and kill them with reactive oxygen species, antimicrobial proteins, and degradative enzymes; they also extrude a chromatin meshwork containing antimicrobial proteins that trap and kill extracellular bacteria, known as neutrophil extracellular traps (NETs).
- Various membrane receptors and ligands are involved in the complex interaction between microbes, cells of the lung parenchyma, and immune defense cells.14
- Histopathology:15 Histologic inflammatory lung changes are best described according to the pattern of infection.
- Lobar pneumonia: Four stages of inflammatory response are classically described, as follows:
- Congestion: This stage is characterized by vascular engorgement, intraalveolar fluid, and numerous bacteria; the lung is heavy, boggy, and red.
- Red hepatization: In this stage, massive confluent exudation develops, with red blood cells, leukocytes, and fibrin filling the alveolar spaces; the affected area appears red, firm, and airless, with a liverlike consistency.
- Gray hepatization: This stage is characterized by progressive disintegration of red blood cells and the persistence of a fibrin exudate.
- Resolution: The consolidated exudate within the alveolar spaces undergoes progressive enzymatic digestion to produce debris that is later resorbed, ingested by macrophages, coughed up, or becomes organized by fibroblasts growing into it.
- Bronchopneumonia: Bronchopneumonia is foci of areas with consolidation resulting from a suppurative, leukocyte-rich exudate that fills the bronchi, bronchioles, and adjacent alveolar spaces. Well-developed lesions may be 3-4 cm in diameter, dry, granular, and grayish-red to yellow, with poorly demarcated margins.
- Interstitial pneumonia
- The typical lung inflammatory response to the atypical bacteria results in an interstitial picture. Alveolar septa become widened and edematous and usually have a mononuclear inflammatory infiltrate of lymphocytes, histiocytes, and plasma cells; neutrophils may also be present in acute cases.
- Pleuritis may result if underlying inflammation extends to the pleural surface of the lung.
- Lobar pneumonia: Four stages of inflammatory response are classically described, as follows:
- Bacterial virulence
- General mechanisms of increased virulence include the following:
- Genetic flexibility allowing the development of resistance to various classes of antibiotics
- Flagellae and other bacterial appendages that facilitate spread of infection
- Capsules resistant to attack by immune defense cells and that facilitate adhesion to host cells
- Quorum sensing systems allow coordination of gene expression based on complex cell-signaling for adaptation to the local cellular environment
- Iron scavenging
- Examples of organism-specific virulence factors are as follows:
- S pneumoniae - Pneumolysin; a multifunctional virulence factor; cytotoxic to respiratory epithelium and endothelium, disrupting pulmonary tissue barriers; directly inhibits immune and inflammatory cells and activates complement, decreasing clearance of the bacteria from the lung16
- P aeruginosa - Pili play important role in attachment to host cells; type III secretion system allows injection of toxins into host cells17
- General mechanisms of increased virulence include the following:
- The role of host resistance: The following deficits in various host defenses and an inability to mount an appropriate acute inflammatory response can predispose patients to infection:14
- Deficits in neutrophil quantity, as in neutropenia
- Deficits in neutrophil quality, as in chronic granulomatous disease
- Deficiencies of complement
- Deficiencies of immunoglobulins
Frequency
United States
In the United States, acute lower respiratory tract infections cause more disease and death than any other infection.14
VAP notably develops in approximately 9-27% of all intubated patients and carries a mortality rate of 30-60%.6,18
The most common etiologies of community-acquired pneumonia (CAP), listed in descending order of frequency are as follows10 :
- Outpatient
- S pneumoniae
- M pneumoniae
- H influenzae
- C pneumoniae
- Respiratory viruses
- Inpatient, non-ICU
- S pneumoniae
- M pneumoniae
- C pneumoniae
- H influenzae
- Legionella species
- Aspiration
- Respiratory viruses
- Inpatient, ICU
- S pneumoniae
- S aureus
- Legionella species
- Gram-negative bacilli
International
Acute lower respiratory tract infections cause a greater burden of disease worldwide than HIV infection, malaria, cancer, or heart attacks.14 The prevalence of various pathogens and epidemiology of disease vary widely between countries and regions, making precise discussion of international disease burden difficult.
Mortality/Morbidity
In 2006, the average length of hospital stay for a patient diagnosed with pneumonia was 5.1 days.19
In 2005, 61,189 people died from pneumonia, with an age-adjusted death rate of 19.7 deaths per 100,000 people. Pneumonia and influenza together were the eighth leading cause of death in the United States.20,21
Race
In 2005, black men were 14% more likely to die from pneumonia compared with white men (26.6 deaths per 100,000 people vs 23 deaths per 100,000 people), whereas black and white women were almost equally likely to die from pneumonia (17.4 deaths per 100,000 people and 18.2 deaths per 100,000 people).20,21
Sex
The number of deaths due to pneumonia has been higher among females since the mid 1980s. However, females have age-adjusted death rates close to 30% lower than those in men because the female population in the United States is larger than the male population. In 2005, the age-adjusted death rates for females and males were 17.9 deaths and 23.9 deaths per 100,000 people, respectively.20,21
Age
Advanced age increases the incidence of and the mortality from pneumonia. For individuals aged 65 years and older, pneumonia and influenza were the sixth leading cause of death in 2005. Close to 90% of deaths due to these diseases occurred in this age group.20,21
Clinical
History
Symptoms11
The presence of cough, particularly cough productive of sputum, is the most consistent presenting symptom. The character of the sputum may suggest a particular pathogen, as follows:
- Rust-colored sputum - Frequently associated with infection by S pneumoniae
- Currant-jelly sputum - Frequently associated with infection by Klebsiella species
- Foul-smelling or bad-tasting sputum - Often produced by anaerobic infections
Chest pain, dyspnea, hemoptysis (when clearly delineated from hematemesis), decreased exercise tolerance, and abdominal pain from pleuritis are also highly indicative of a pulmonary process
Nonspecific symptoms such as fever, rigors or shaking chills, and malaise are common. Other nonspecific symptoms that may be seen with pneumonia include myalgias, headache, nausea, vomiting, diarrhea, and altered sensorium.
History of various exposures can be helpful in determining possible etiologies and the likelihood of bacterial pneumonia, as follows:
- Exposure to contaminated air-conditioning or water systems -Legionella species
- Exposure to overcrowded institutions (eg, jails, homeless shelters) -S pneumoniae, Mycobacteria, Mycoplasma, Chlamydophila
- Exposure to various types of animals
- Cats, cattle, sheep, goats -C burnetii, B anthracis (cattle hide)
- Turkeys, chickens, ducks, or other birds -C psittaci
- Rabbits, rodents -F tularensis, Y pestis
Aspiration risks
As previously discussed, patients at increased risk of aspiration are also at increased risk of developing pneumonia secondarily; factors are as follows:
- Alcoholism
- Altered mental status
- Anatomic abnormalities, congenital or acquired
- Dysphagia
- GERD
- Seizure disorder
Additional host factors
As always, a thorough interview and determination of past medical history is of utmost utility; inquire about the following:
- Comorbid conditions
- Previous surgeries
- Possibility of immunosuppression
- Social and sexual history
- Family history
- Medication history
- Allergy history
Physical
Physical examination findings may vary depending on the type of organism, severity of infection, coexisting host factors, and the presence of complications.11,22
Signs
- Hyperthermia (fever, typically >38°C) or hypothermia (<35°C)
- Tachypnea (>18 respirations/min)
- Use of accessory respiratory muscles
- Tachycardia (>100 bpm) or bradycardia (<60 bpm)
- Central cyanosis
- Altered mental status
- Adventitious breath sounds, such as rales/crackles, rhonchi or wheezes
- Decreased intensity of breath sounds
- Egophony
- Whispering pectoriloquy
- Dullness to percussion
- Tracheal deviation
- Lymphadenopathy
- Examination findings possibly indicating a specific etiology for consideration
- Bradycardia -Legionella
- Periodontal disease - Anaerobic and/or polymicrobial infection
- Bullous myringitis -Mycoplasma pneumoniae
- Physical evidence of risk for aspiration (eg, decreased gag reflex)
- Cutaneous nodules (especially in the setting of CNS findings) -Nocardia
Causes
See "Bacterial pathogens of pneumonia and some notable features" in Pathophysiology.
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Further Reading
Keywords
bacterial pneumonia, pneumonia, pneumococcus, Streptococcus pneumoniae, S pneumoniae, Haemophilus influenzae, H influenzae, Staphylococcus aureus, S aureus, Legionella, Legionella pneumophila, Mycoplasma, Mycoplasma pneumoniae, Chlamydophila psittaci, Coxiella burnetii, C burnetii, Pseudomonas, Klebsiella, Klebsiella pneumoniae, K pneumoniae, Moraxella catarrhalis, M catarrhalis, Nocardia, Escherichia coli, Enterobacter, Serratia species, Bacteroides, Peptostreptococcus, Fusobacterium species, hospital-acquired pneumonia, community-acquired pneumonia, CAP, nosocomial pneumonia, viral pneumonia, typical pneumonia, atypical pneumonia, lobular pneumonia, lobar pneumonia, bronchial pneumonia
