Bacterial Pneumonia 

Updated: Aug 22, 2019
Author: Justina Gamache, MD; Chief Editor: Guy W Soo Hoo, MD, MPH 

Overview

Practice Essentials

Bacterial pneumonia (see the image below) is caused by a pathogenic infection of the lungs and may present as a primary disease process or as the final, fatal disorder primarily in an individual who is already debilitated. The most consistent presenting symptom of bacterial pneumonia is cough productive of sputum. Antibiotic treatment is the mainstay of drug therapy for bacterial pneumonia.

Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with right upper lobe pneumonia. Note the increased anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary disease (COPD).

Signs and symptoms of bacterial pneumonia

Cough, particularly cough productive of sputum, is the most consistent presenting symptom of bacterial pneumonia and may suggest a particular pathogen, as follows:

  • Streptococcus pneumoniae: Rust-colored sputum

  • Pseudomonas, Haemophilus, and pneumococcal species: May produce green sputum

  • Klebsiella species pneumonia: Red currant-jelly sputum

  • Anaerobic infections: Often produce foul-smelling or bad-tasting sputum

Signs of bacterial pneumonia may include the following:

  • Hyperthermia (fever, typically >38°C)[1] 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

Physical findings may include the following:

  • Adventitious breath sounds, such as rales/crackles, rhonchi, or wheezes

  • Decreased intensity of breath sounds

  • Egophony

  • Whispering pectoriloquy

  • Dullness to percussion

  • Tracheal deviation

  • Lymphadenopathy

  • Pleural friction rub

Examination findings that may indicate a specific etiology include the following:

  • Bradycardia: May indicate a Legionella etiology

  • Periodontal disease: May suggest an anaerobic and/or polymicrobial infection

  • Cutaneous nodules: May suggest Nocardia infection

  • Decreased gag reflex: Suggests risk for aspiration

See Clinical Presentation for more detail.

Diagnosis of bacterial pneumonia

Severity assessment

Tools to assess the severity of disease and risk of death include the PSI/PORT (ie, pneumonia severity index/Patient Outcomes Research Team score), the CURB-65 (ie, confusion, urea, respiratory rate, blood pressure, and age >65 years) system, and the APACHE (ie, acute physiology and chronic health evaluation), among others.

The following laboratory tests are also useful for assessing illness severity:

  • Serum chemistry panel

  • Arterial blood gas (ABG) determination

  • Venous blood gas determination (central venous oxygen saturation)

  • Complete blood cell (CBC) count with differential

  • Serum free cortisol value

  • Serum lactate level

Sputum evaluation

Sputum Gram stain and culture should be performed before initiating antibiotic therapy. A single predominant microbe should be noted at Gram staining, although mixed flora may be observed with anaerobic infection caused by aspiration.

Imaging studies

  • Chest radiography: The criterion standard for establishing the diagnosis of pneumonia

  • Chest computed tomography scanning

  • Chest ultrasonography

Bronchoscopy

Lung tissue can be visually evaluated and bronchial washing specimens can be obtained with the aid of a fiberoptic bronchoscope. Protected brushings and bronchoalveolar lavage (BAL) can be performed for fluid analysis and cultures.

Thoracentesis

This is an essential procedure in patients with a parapneumonic pleural effusion. Analysis of the fluid allows differentiation between simple and complicated effusions.

Pathogen-specific tests

  • Urine assays

  • Sputum, serum, and/or urinary antigen tests

  • Immune serologic tests

Histologic examination

Histologic inflammatory lung changes vary according to whether the patient has lobar pneumonia, bronchopneumonia, or interstitial pneumonia.[2]

See Workup for more detail.

Management of bacterial pneumonia

The mainstay of drug therapy for bacterial pneumonia is antibiotic treatment. First-line antimicrobials for S pneumoniae, the most prevalent cause of bacterial pneumonia, are, for the penicillin-susceptible form of the bacterium, penicillin G and amoxicillin. For the penicillin-resistant form of S pneumoniae, first-line agents are chosen on the basis of sensitivity.

Supportive measures include the following:

  • Analgesia and antipyretics

  • Chest physiotherapy

  • Intravenous fluids (and, conversely, diuretics), if indicated

  • Pulse oximetry with or without cardiac monitoring, as indicated

  • Oxygen supplementation

  • Positioning of the patient to minimize aspiration risk

  • Respiratory therapy, including treatment with bronchodilators and N-acetylcysteine

  • Suctioning and bronchial hygiene

  • Ventilation with low tidal volumes (6 mL/kg of ideal body weight) in patients requiring mechanical ventilation secondary to bilateral pneumonia or acute respiratory distress syndrome (ARDS)[3]

  • Systemic support: May include proper hydration, nutrition, and mobilization

See Treatment and Medication for more detail.

Background

Pneumonia can be generally defined as an infection of the lung parenchyma, in which consolidation of the affected part and a filling of the alveolar air spaces with exudate, inflammatory cells, and fibrin is characteristic.[4] Infection by bacteria or viruses is the most common cause, although infection by other micro-orgamisms such as rickettsiae, fungi and yeasts, and mycobacteria may occur.[4] (See the images below.)

A 53-year-old patient with severe Legionella pneum A 53-year-old patient with severe Legionella pneumonia. Chest radiograph shows dense consolidation in both lower lobes.
A 40-year-old patient with Chlamydia pneumonia. Ch A 40-year-old patient with Chlamydia pneumonia. Chest radiograph shows multifocal, patchy consolidation in the right upper, middle, and lower lobes.
A 38-year-old patient with Mycoplasma pneumonia. C A 38-year-old patient with Mycoplasma pneumonia. Chest radiograph shows a vague, ill-defined opacity in the left lower lobe.

Bacterial pneumonia is caused by a pathogenic infection of the lungs and may present as a primary disease process or as the final coup de grace in the individual who is already debilitated. For example, a historical review of the 1918-19 influenza pandemic suggests that the majority of deaths were not a direct effect of the influenza virus, but they were from bacterial coinfection.[5]

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. A major part of what distinguishes these various categories from each other is the varying risk of exposure to multidrug-resistant (MDR) organisms.[6, 7, 8, 9, 10, 11]

Anatomic or radiologic distribution of pneumonia includes the following (see Chest Radiography for details):

  • Lobar - Known as focal or nonsegmental pneumonia (see the images below)

  • Multifocal/lobular (bronchopneumonia)

  • Interstitial (focal diffuse)

    Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with right upper lobe pneumonia. Note the increased anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary disease (COPD).
    Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with bilateral lower lobe pneumonia. Note the spine sign, or loss of progression of radiolucency of the vertebral bodies
    Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with early right middle lobe pneumonia.

The setting of pneumonia includes the community, institutional (healthcare/nursing home setting), and nosocomial (hospital).

Community-acquired pneumonia

Community-acquired pneumonia (CAP) is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital.

Go to Community-Acquired Pneumonia for complete information on this topic.

Institutional-acquired pneumonia

Institutional-acquired pneumonia (IAP) includes HCAP and nursing home–associated pneumonia (NHAP).

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 two 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 epidemiologic associations with infection in nonhospital healthcare settings.[4] 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.

It is important to note that nursing home patients with pneumonia are less likely to present with classic signs and symptoms of the typical pneumonia presentation, such as fever, chills, chest pain, and productive cough, but instead these individuals often have delirium and altered mental status.[6, 7]

Go to Nursing Home Acquired Pneumonia for complete information on this topic.

The concept of HCAP (including NHAP) has been called into question in the 2016 Infectious Diseases Society of America (IDSA) and American Thoracic Society (ATS) guidelines.[12] Based on a 2014 meta-analysis of 24 studies, it was found that the concept of HCAP is predominantly based on low-quality evidence confounded by publication bias and does not accurately identify multidrug-resistant organisms. After adjusting for age and comorbidities, patients within this category did not have an increased risk of mortality.[13] Based on this meta-analysis, the 2016 IDSA and ATS guidelines have called for the removal of the concept of HCAP,[12] encouraging patients previously grouped under this category to be treated as if they have CAP, with guidance of hospital-specific antibiograms and local resistance patterns.

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 hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (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.[14]

Go to Ventilator-Associated Pneumonia and Nosocomial Pneumonia for complete information on these topics.

Hospital-acquired pneumonia

HAP is defined as pneumonia that develops at least 48 hours after admission to a hospital and is characterized by increased risk of exposure to MDR organisms,[6] as well as gram-negative organisms.[15] Risk factors for exposure to such organisms in HAP include the following[6] :

  • Antibiotic therapy within 90 days of the hospital-acquired infection

  • Current length of hospitalization of five 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

Common mechanisms for the acquisition of pneumonia include ventilator use and aspiration.

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 that cause VAP are the same as those for HAP.[6, 8] VAP may occur in as many as 10-20% of patients who are on ventilators for more than 48 hours.[16]

Go to Ventilator-Associated Pneumonia for complete information on this topic.

Aspiration pneumonia

Aspiration pneumonia develops after the inhalation of oropharyngeal secretions and colonized organisms. Although 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.

Critically ill patients are at notably increased risk of aspiration due to the following:

  • 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.[17] However, recurrence of aspiration pneumonia is common unless the risk factors for underlying aspiration are treated or minimized.

Go to Aspiration Pneumonia for complete information on this topic.

Pathophysiology

The causes for the development of pneumonia are extrinsic or intrinsic, and various bacterial causes are noted. Extrinsic factors include exposure to a causative agent, exposure to pulmonary irritants, or direct pulmonary injury. Intrinsic factors are related to the host. Loss of protective upper airway reflexes allows aspiration of contents from the upper airways into the lung. Various causes for this loss include altered mental status due to intoxication and other metabolic states and neurologic causes, such as stroke and endotracheal intubation.

Bacteria from the upper airways or, less commonly, from hematogenous spread, find their way to the lung parenchyma. Once there, a combination of factors (including virulence of the infecting organism, status of the local defenses, and overall health of the patient) may lead to bacterial pneumonia. The patient may be made more susceptible to infection because of an overall impairment of the immune response (eg, human immunodeficiency virus [HIV] infection, chronic disease, advanced age) and/or dysfunction of defense mechanisms (eg, smoking, chronic obstructive pulmonary disease [COPD], tumors, inhaled toxins, aspiration). Poor dentition or chronic periodontitis is another predisposing factor.

Thus, 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. These neutrophils 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.[18]

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

The following are examples of organism-specific virulence factors:

  • Streptococcus pneumoniae – Pneumolysin, a multifunctional virulence factor, is cytotoxic to respiratory epithelium and endothelium by disrupting pulmonary tissue barriers. This factor directly inhibits immune and inflammatory cells and activates complement, decreasing the clearance of the bacteria from the lung.[19]

  • Pseudomonas aeruginosa - Pili play important role in the attachment to host cells. A type III secretion system allows injection of toxins into host cells.[20]

Host resistance

Deficits in various host defenses and an inability to mount an appropriate acute inflammatory response can predispose patients to infection, as follows[18] :

  • Deficits in neutrophil quantity, as in neutropenia

  • Deficits in neutrophil quality, as in chronic granulomatous disease

  • Deficiencies of complement

  • Deficiencies of immunoglobulins

Viral infection

With the recent H1N1 influenza virus pandemic, it is important to address the role that viral infection can have in bacterial pneumonia.

The association between infection with influenza virus and subsequent bacterial pneumonia became particularly apparent following the 1918 influenza pandemic, during which approximately 40-50 million people died.[21] Historical investigations and current researchers argue that the vast majority of pulmonary-related deaths from past pandemic influenza viruses, most notably the pandemic of 1918, ultimately resulted from bacteriologic secondary or coinfection and poorly understood interactions between the infecting viral and bacterial organisms.[22] Although influenza virus is the most commonly thought of agent in this co-infective context, other respiratory viruses, such as respiratory syncytial virus (RSV), parainfluenza viruses, adenovirus, and rhinoviruses, may also predispose to secondary bacterial infection.[21]

The classic explanation behind the viral-bacterial interplay focuses on the disruption of the respiratory epithelium by the virus, providing an opportinistic environment for bacterial infection. However, evidence depicts much more complex and possibly synergistic interactions between viruses and bacteria, including alteration of pulmonary physiology, downregulation of the host immune defense, changes in expression of receptors to which bacteria adhere, and enhancement of the inflammatory process.[21]

Etiology of Bacterial Pneumonia

Although pneumonia may be caused by myriad pathogens, a limited number of agents are responsible for most cases,[3, 23, 24, 25] Most authors categorize bacterial pneumonias by their infectious agents, which include pneumococcal agents; Haemophilus influenzae; Klebsiella, Staphylococcus, and Legionella species; gram-negative organisms; and aspirated micro-organisms. Microaspiration of organisms that colonize the upper respiratory tract and mucosal surfaces is probably the most common mode of infection. Some agents, notably Staphylococcus species, may be spread hematogenously.

Risk factors

Coinfection with H1N1 influenza increases the risk of secondary bacterial pneumonia, with S pneumoniae the most likely coinfection.[26] However, pregnant patients with H1N1 influenza in the 2009 pandemic were at increased risk of developing secondary Klebsiella pneumonia with poor clinical outcome.[27]

Other risk factors include local lung pathologies (eg, tumors, chronic obstructive pulmonary disease [COPD], bronchiectasis), chronic gingivitis and periodontitis, and smoking which impairs resistance to infection. Furthermore, any individual with an altered sensorium (eg, seizures, alcohol or drug intoxication) or central nervous system (CNS) impairment (eg, stroke) may have a reduced gag reflex, which allows aspiration of stomach or oropharyngeal contents and contributes to the development of aspiration pneumonias.

Typical organisms

Although several of the organisms discussed in this section may be implicated in pneumonia, only a few of them are responsible for the vast majority of cases.

Gram-positive bacteria that can cause pneumonia include the following:

  • Streptococcus pneumoniae: This organism is a facultative anaerobe identified by its chainlike staining pattern. Pneumococcosis is by far the most common cause of typical bacterial pneumonia.

  • Staphylococcus aureus: S aureus is a facultative anaerobe identified by its clusterlike staining pattern. S aureus pneumonia is observed in intravenous drug abusers (IVDAs) and individuals with debilitating disorders. In patients who abuse intravenous drugs, the infection probably is spread hematogenously to the lungs from contaminated injection sites. Methicillin-resistant S aureus (MRSA) has had a large impact on empiric antibiotic choices at many institutions.

  • Enterococcus (E faecalis, E faecium): These organisms are group D streptococci that are well-known normal gut florae that 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 gastrointestinal (GI) tract and can colonize the oral cavity in patients with periodontal disease. A israelii is known to form abscesses and sulfur granules.

  • Nocardia asteroides: N asteroides is a weakly gram-positive, partially acid-fast bacillus (AFB) that forms beaded, branching, thin 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 pneumonias occur most often in individuals who are debilitated, immunocompromised, or recently hospitalized. Individuals living in long-term care facilities where other residents are intubated are also at risk for these infections. Gram-negative bacteria include the following:

  • 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 that can lead to an aggressive, necrotizing, lobar pneumonia. Patients with chronic alcoholism, diabetes, or COPD are at increased risk for infection with this organism.

  • Haemophilus influenzae: H influenzae is an aerobic bacillus that comes in both encapsulated and nonencapsulated forms. Several major subtypes have been identified, which have varying levels of pathogenicity. Encapsulated type B (HiB) is known to be particularly virulent, although routine vaccination against this subtype has decreased the prevalence of severe disease caused by H influenzae. Infection with this bacteria is more common in patients with COPD.

  • 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 ventilator-associated pneumonia (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 and that 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 biologic weapon.[28]

  • Bacillus anthracis: B anthracis is the agent responsible for inhalational anthrax.

  • Yersinia pestis: Y pestis infection is better known as the black plague. It is the most commonly accepted cause of the pandemic known as the bubonic plague. This organism can also cause the pneumonic plague. The pneumonic plague causes a lung infection by the direct inhalation of aerosolised plague bacteria or, secondary, when the organism spreads to the lungs from the bloodstream. Pneumonic plague is, therefore, not exclusively vector-borne like bubonic plague. Instead, it can be spread from person to person. Other members of the Yersinia family are responsible for a wide variety of infectious presentations.

Atypical organisms

Atypical organisms are generally associated with a milder form of pneumonia, the so-called "walking pneumonia." A feature that makes these organisms atypical is the inability to detect them on Gram stain or to cultivate them in standard bacteriologic media.[23, 3] Atypical organisms include the following:

  • Mycoplasma species: The mycoplasmas are the smallest known free-living organisms in existence. These organisms lack cell walls (and therefore are not apparent after Gram stain) but have protective 3-layered cell membranes.

  • Chlamydophila species (C psittaci, C 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 and are known to grow in complex water distribution systems. Institutional water contamination is frequently noted in endemic outbreaks. Legionellapneumophila is the causative agent of the majority of Legionnaires' disease. Other Legionella species are known to infect the lower respiratory system.

  • 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.

Anaerobic organisms

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.

Epidemiology

In the United States, acute lower respiratory tract infections cause more disease and death than any other infection.[18] In fact, these infections also cause a greater burden of disease worldwide than human immunodeficiency virus (HIV) infection, malaria, cancer, or heart attacks.[18] The prevalence of various pathogens and epidemiology of disease vary widely between countries and regions, making precise discussion of international disease burden difficult.

More than three million cases occur annually in the United States. Pneumonia is more prevalent during the winter months and in colder climates. This condition is most likely from viral upper and lower respiratory infections, which increase in winter and result in impaired host defenses to bacterial superinfection.

Community-acquired pneumonia

The most common etiologies of community-acquired pneumonia (CAP) in the outpatient setting are as follows (in descending order of frequency):[3] S pneumoniae, M pneumoniae, H influenzae, C pneumoniae, and respiratory viruses.

The most common etiologies of CAP in the non–intensive care unit (ICU) inpatient setting, in descending order of frequency, are as follows:[3] S pneumoniae, M pneumoniae, C pneumoniae, H influenzae, Legionella species, aspiration, and respiratory viruses. Legionella pneumophila infections tend to occur sporadically and in local epidemic clusters. These infections usually arise in the summer and fall and may be found in the water condensed from air conditioning systems.

The most common etiologies of CAP in the ICU inpatient setting, in descending order of frequency, are as follows[3] : S pneumoniae, S aureus, Legionella species, and Gram-negative bacilli.

Ventilator-associated pneumonia (VAP) notably develops in approximately 9-27% of all intubated patients and carries a mortality rate of 30-60%.[8, 29]

Race, sex, and age

Black men (26.6 deaths per 100,000 population) are more likely to die from pneumonia compared with white men (23 deaths per 100,000 population), whereas black (17.4 deaths per 100,000 population) and white women (18.2 deaths per 100,000 population) are almost equally likely to die from pneumonia.[30, 31]

The incidence of pneumonia is greater in males than in females but the total 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. The age-adjusted death rates for females have been reported as 17.9 deaths per 100,000 population and 23.9 deaths per 100,000 population for males.[30, 31]

Advanced age increases the incidence of and the mortality from pneumonia. Comorbidity and a diminished immune response and defense against aspiration increase the risk of bacterial pneumonia. For individuals aged 65 years and older, pneumonia and influenza were the sixth leading cause of death in 2005.[30, 31] Close to 90% of deaths due to pneumonia and influenza occurred in this age group. In a 20-year US study, the average overall mortality rate in pneumococcal pneumonia with bacteremia was 20.3%. Patients older than 80 years of age had the highest mortality rate, which was 37.7%.[32]

Prognosis

Generally, the prognosis is good in otherwise healthy patients with uncomplicated pneumonia. Advanced age, aggressive organisms (eg, Klebsiella, Legionella, resistant S pneumoniae), comorbidity, respiratory failure, neutropenia, and features of sepsis, alone or in combination, increase morbidity and mortality. Left untreated, pneumonia may have an overall mortality rate of more than 30%.

Even with appropriate treatment, the risk of mortality may be high if the host is ill or infirm. The Pneumonia Severity Index (PSI) may be used as a guide to determine a patient's mortality risk, but it tends to overestimate the actual risk in many cases (see Pneumonia severity index under Risk Stratification in Clinical Presentation). Particularly virulent organisms, such as Klebsiella and Legionella species, may confer a higher mortality rate.

In a study looking at microbial etiologies of CAP, S pneumoniae was present in the highest total number of deaths. However, gram-negative enteric bacilli, Pseudomonas, Staphylococcus aureus, and mixed etiologies had the highest mortality rates in those effected.[33]

Morbidity may include destruction of lung tissue from infection with subsequent scarring. Affected areas may be incapable of gas exchange, reducing respiratory reserve. In a patient with pre-existing respiratory disease, the onset of bacterial pneumonia may result in a downward spiral of infections, further impairment of respiratory status, and repeated infections owing to reduced local and systemic immune responses. Bronchiectasis may be a sequela of bacterial pneumonia. Infections with Staphylococcus and Klebsiella organisms may result in subsequent bronchiectasis, especially if treatment is delayed.

Destroyed alveoli and small-to-medium airways may be replaced by dilated blind saccules filled with purulent material. Ongoing, chronic inflammation usually occurs in the surrounding area and may destroy local adjacent lung tissue over time. Empyema and lung abscess may occur as direct complications of bacterial pneumonia. Pneumonia has been associated with increased incidence of placental abruption in pregnant patients.

Patient Education

Patients should be encouraged to stop smoking, to avoid drinking alcohol to intoxication, and to keep their teeth in good repair. In addition, instruct patients at risk to receive appropriate influenza and pneumococcal immunizations.

Patients, particularly elderly and debilitated patients, should be instructed to seek prompt care should symptoms of dyspnea or fever and rigors develop.

For patient education information, see the Lungs Center, as well as Bacterial Pneumonia and Viral Pneumonia.

 

Presentation

History

During the intake history, the patient’s potential exposures, aspiration risks, host factors, and symptoms should be reviewed.

Potential exposures

A history of various exposures, such as travel, animal, occupational, and environmental 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. Associated factors are as follows:

  • Alcoholism

  • Altered mental status

  • Anatomic abnormalities, congenital or acquired

  • Drug use

  • Dysphagia

  • Gastroesophageal reflux disease (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 (eg, asthma, COPD, smoking, and a compromised immune system are risk factors for H influenzae infection.)

  • Previous surgeries

  • Possibility of immunosuppression

  • Social and sexual history

  • Family history

  • Medication history

  • Allergy history

Symptoms

The clinical presentation of bacterial pneumonia varies. Sudden onset of symptoms and rapid illness progression are associated with bacterial pneumonias. 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.

The presence of cough, particularly cough productive of sputum, is the most consistent presenting symptom. Although not diagnostic of a particular causative agent, the character of the sputum may suggest a particular pathogen, as follows:

  • S pneumoniae is classically associated with a cough productive of rust-colored sputum.

  • Pseudomonas, Haemophilus, and pneumococcal species may produce green sputum.

  • Klebsiella species pneumonia is classically associated with a cough productive of red currant-jelly sputum.

  • Anaerobic infections often produce foul-smelling or bad-tasting sputum.

Nonspecific symptoms such as fever, rigors or shaking chills, and malaise are common. For unclear reasons, the presence of rigors may suggest pneumococcal pneumonia more often than pneumonia caused by other bacterial pathogens.[34] Other nonspecific symptoms that may be seen with pneumonia include myalgias, headache, abdominal pain, nausea, vomiting, diarrhea, anorexia and weight loss, and altered sensorium.[24]

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.

Pneumonia from H influenzae most commonly arises in the winter and early spring. This pneumonia is more often associated with hosts who are debilitated.

Patients with Legionella pneumonia often present with mental status changes or diarrhea. Patients may develop hemoptysis or pulmonary cavitations. In addition, unlike other pneumonias, more than 50% of the time Legionella pneumonia has gastrointestinal (GI) symptoms associated with it, such as anorexia, nausea, vomiting, and diarrhea. Hyponatremia is often noted.

L pneumophila seems to have 2 forms: Pontiac fever and frank Legionella pneumonia. Pontiac fever has a viruslike presentation, with malaise, fever and/or chills, myalgias, and headache. This form of Legionella pneumonia usually subsides without sequelae. However, frank Legionella pneumonia is very aggressive, with a mortality rate as high as 75% unless treatment begins rapidly. This form typically occurs in individuals who are elderly and debilitated, as well as in smokers and those with COPD, alcoholism, immunocompromise, or have experienced trauma.

Physical Examination

Physical examination findings may vary, depending on the type of organism, severity of infection, coexisting host factors, and the presence of complications.[24, 35]

Signs of bacterial pneumonia may include the following:

  • Hyperthermia (fever, typically >38°C)[1] 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

Physical findings may include the following:

  • Adventitious breath sounds, such as rales/crackles, rhonchi, or wheezes

  • Decreased intensity of breath sounds

  • Egophony

  • Whispering pectoriloquy

  • Dullness to percussion

  • Tracheal deviation

  • Lymphadenopathy

  • Pleural friction rub

Examination findings that may indicate a specific etiology for consideration are as follows:

  • Bradycardia may indicate a Legionella etiology.

  • Periodontal disease may suggest an anaerobic and/or polymicrobial infection.

  • Bullous myringitis may very rarely indicate Mycoplasma pneumoniae infection (largely disproven).

  • Physical evidence of risk for aspiration may include a decreased gag reflex.

  • Cutaneous nodules, especially in the setting of central nervous system (CNS) findings may suggestion Nocardia infection.

Risk Stratification

Severity-of-illness scores or prognostic models, such as the CURB-65 criteria or the Pneumonia Severity Index (PSI) can be used to help identify patients that may be candidates for outpatient treatment and those that may require admission (see below). The Infectious Disease Society of America (IDSA) and American Thoracic Society (ATS) proposed guidelines and criteria to determine the severity of community-acquired pneumonia (CAP), which would affect whether inpatient treatment would occur on the ward or require ICU care.[36] Although many of these predictive models were originally designed for assessment of CAP, a retrospective cohort study determined that they may also be applicable to HCAP.[37]

CURB-65

CURB-65 is a scoring system developed from a multivariate analysis of 1068 patients that identified various factors that appeared to play a role in patient mortality.[38] One point is given for the presence of each of the following:

  • C onfusion – Altered mental status

  • U remia – Blood urea nitrogen (BUN) level greater than 20 mg/dL

  • R espiratory rate –30 breaths or more per minute

  • B lood pressure – Systolic pressure less than 90 mm Hg or diastolic pressure less than 60 mm Hg

  • Age older than 65 years

Current guidelines suggest that patients may be treated in an outpatient setting or may require hospitalization according to their CURB-65 score, as follows:

  • Score of 0-1 – Outpatient treatment

  • Score of 2 – Admission to medical ward

  • Score of 3 or higher – Admission to intensive care unit (ICU)

The percentage of mortality at 30 days associated with the various CURB-65 scores increases with higher scores. The drastic increase in mortality between scores of 2 and 3 highlights the likely requirement for ICU admission in patients with a score of 3 or higher, as shown below:

  • Score of 0 – 0.7% mortality

  • Score of 1 – 2.1% mortality

  • Score of 2 – 9.2% mortality

  • Score of 3 – 14.5% mortality

  • Score of 4 – 40% mortality

  • Score of 5 – 57% mortality

Pneumonia severity index

The PSI, also known as the PORT score (for the study by which it was validated), is a prediction rule for mortality based on characteristics derived from cohorts of patients hospitalized with pneumonia.[39] For each of the various characteristics, a predetermined value of points is assigned. In a retrospective cohort comparison of different predictive models applied to HCAP, the PSI had the highest sensitivity in predicting mortality. However, alternative tools, including the IDSA/ATS, SCAP, and SMART-COP (mentioned below), are considered easier to calculate.[37]

Demographic factors are scored as follows:

  • Age, men – Starting point value is age in years

  • Age, women – Starting point value is age in years minus 10 points

  • Nursing home resident – Add 10 points

Coexisting illnesses are scored as follows:

  • Neoplasia – Add 30 points

  • Liver disease – Add 20 points

  • Congestive heart failure, cerebrovascular disease, renal disease – Add 10 points for each

Physical examination findings are scored as follows:

  • Altered mental status – Add 20 points

  • Respiratory rate of 30 breaths or more per minute – Add 20 points

  • Systolic blood pressure less than 90 mmHg – Add 20 points

  • Temperature less than 35°C or that is 40°C or higher – Add 15 points

  • Pulse greater than 125 bpm – Add 10 points

Laboratory and radiographic findings are scored as follows:

  • Arterial pH less than 7.35 – Add 30 points

  • BUN value of 30 mg/dL or greater – Add 20 points

  • Sodium level less than 130 mmol/L – Add 20 points

  • Glucose level of 250 mg/dL or greater – Add 10 points

  • Hematocrit value less than 30% – Add 10 points

  • Partial arterial pressure (PaO2) less than 60 mm Hg or peripheral oxygen saturation (SpO2) less than 90% while breathing room air – Add 10 points

  • Pleural effusion – Add 10 points

The combined total points make up the risk score, which stratifies patients into 5 PSI mortality risk classes, as follows:

  • 0-50 points = Class I (0.1% mortality)

  • 51-70 points = Class II (0.6% mortality)

  • 71-90 points = Class III (0.9% mortality)

  • 91-130 points = Class IV (9.3% mortality)

  • More than 130 points = Class V (27% mortality)

Current guidelines suggest that patients may be treated in an outpatient setting or may require hospitalization depending on their PSI risk class, as follows:

  • Classes I and II – Outpatient management

  • Class III – Admission to an observation unit or for short hospital stay

  • Classes IV and V – Treatment in inpatient setting

The Agency for Healthcare Research and Quality (AHRQ) has provided a PSI calculator.[40]

It is important to remember that objective criteria and scores should be used as guides only and should always be supplemented with physician determination of the patient's therapeutic needs. The risks and benefits of hospitalization should be weighed carefully, because hospitalization can put patients at additional risk (eg, thromboembolic events, nosocomial superinfection). When a pneumonia is due to mixed etiologies, it is often underestimated by severity scores.[33]

IDSA/ATS CAP criteria

Prediction rules like the CURB-65 and PSI have proven useful for standardizing clinical assessments and identifying low-risk patients who may be appropriate candidates for outpatient therapy, but they have been less useful for discriminating between moderate (ward-appropriate) and high-risk (ICU-appropriate) patients.[41]

The IDSA/ATS criteria for severe community-acquired pneumonia (CAP) are composed of both major and minor criteria. Although the major criteria indicate clear need for ICU-level care, the minor criteria for defining severe CAP have been validated for the use of differentiating between patients requiring ward-level versus ICU-level care.[41, 36, 42]

These criteria are particularly helpful in identifying those patients who are appropriate for admission to the ICU but who do not meet the major criteria of requiring mechanical ventilation or vasopressor support.

The presence of three of the following minor criteria indicates severe CAP and suggests the likely need for ICU-level care:

  • Respiratory rate of 30 breaths or more per minute

  • Ratio of PaO2 to fraction of inspired oxygen (ie, PaO2/FiO2) of 250 or less

  • Need for noninvasive ventilation (bilevel positive airway pressure [BiPAP] or continuous positive airway pressure [CPAP])

  • Multilobar infiltrates

  • Confusion/disorientation

  • Uremia (BUN 20 mg/dL or greater)

  • Leukopenia (white blood cell [WBC] count less than 4000 cells/µL)

  • Thrombocytopenia (platelet count less than 100,000/µL)

  • Hypothermia (core temperature less than 36°C)

  • Hypotension requiring aggressive fluid resuscitation

The major criteria are as follows:

  • Invasive mechanical ventilation

  • Septic shock requiring vasopressor support

Direct admission to an ICU is mandated for any patient with septic shock and a requirement for intravenous vasopressors support or with acute respiratory failure requiring intubation and mechanical ventilation.

Biological markers

Over the past 10 years, great enthusiasm has been noted regarding the potential of biological markers, such as C-reactive protein (CRP) and procalcitonin (PCT), for the diagnosis and prognostication of pneumonia. PCT appears to be promising, especially as a prognosticator.[43]

Other scoring models

Multiple other scoring models exist that can be used to aid in the prediction of mortality in severe illness (namely in the ICU setting), including the acute physiology and chronic health evaluation (APACHE II) score,[44] simplified acute physiology score (SAPS II),[45] and sepsis-related organ failure assessment (SOFA) score.[46]

Whereas most scoring models have been used for predicting outcomes in patients carrying a diagnosis of CAP, the systolic blood pressure, oxygenation, age, respiratory rate (SOAR) model has been validated for predicting 30-day mortality in patients hospitalized with nursing home-acquired pneumonia (NHAP).[47]

Still other prediction models regarding pneumonia severity and outcomes are currently being explored and developed, such as the Spanish CURXO-80 tool[48] ; predisposition, insult, response, and organ dysfunction (PIRO) tool[49] ; and systolic blood pressure, multilobar involvement, albumin level, respiratory rate, tachycardia, confusion, oxygenation and arterial pH (SMART-COP) tool.[50]

Complications

Potential complications of bacterial pneumonia include the following:

  • Destruction and fibrosis/organization of lung parenchyma with scarring

  • Bronchiectasis

  • Necrotizing pneumonia

  • Frank cavitation

  • Empyema

  • Pulmonary abscess

  • Respiratory failure

  • Acute respiratory distress syndrome

  • Ventilator dependence

  • Superinfection

  • Meningitis

  • Death

Parapneumonic pleural effusions and empyema

Parapneumonic effusions are common complications of bacterial pneumonia. These pleural effusions occur adjacent to a bacterial pneumonia, resulting from migration of excess interstitial lung fluid across the visceral pleura. Small-volume parapneumonic effusions typically resolve with treatment of the bacterial pneumonia and thus do not require drainage. However, pleural effusions greater than 10mm on lateral decubitus radiographic view should undergo thoracentesis and pleural fluid analysis, Gram stain, and culture to further guide antibiotic selection. Parapneumonic effusions with radiographic evidence of loculated or thickened pleura suggestive of empyema, or pleural fluid pH less than 7.2 or a glucose value less than 60, typically require thoracostomy tube drainage and possible thorascopic debridement via thoracic surgery. Empiric antibiotics for bacterial pneumonias complicated by empyema should include anaerobic coverage, as anaerobic bacteria are often cultured from empyemas.[51]

Go to Parapneumonic Pleural Effusions and Empyema Thoracis  for complete information on this topic.

 

DDx

Diagnostic Considerations

Remember that the most prevalent causative organism in bacterial pneumonia is pneumococcus regardless of the host. Empiric therapy must be selected with this organism in mind.

Because the episode of aspiration is usually not witnessed, the diagnosis is inferred when a patient at risk of aspiration develops evidence of a radiographic infiltrate in characteristic anatomic pulmonary locations or bronchopulmonary segments.

Always consider the possibility of Legionella infection, because delayed treatment significantly increases mortality.

Despite the frequency of pneumonia and the large body of research and literature surrounding it, controversy remains regarding certain aspects of the evaluation and management of pneumonia. Much emphasis has been placed on the utility of diagnostic testing versus the role of empiric treatment. The following three aspects of disease are important in the management of pneumonia, in which diagnostic testing can play a pivotal role:

  • Determining the presence of pneumonia

  • Assessing disease severity at the time of presentation

  • Identifying the causative agent

Distinguishing pneumonia from other pulmonary pathologies, such as acute COPD or asthma exacerbation, can often present a significant challenge, particularly in patients with these underlying lung diseases. C-reactive protein (CRP) and procalcitonin values may help in distinguishing infectious pneumonia from noninfectious underlying disease exacerbations.[52]

Differentiation between CAP, healthcare-associated pneumonia (HCAP), hospital-acquired pneumonia (HAP), and other pulmonary pathology at presentation is important for several reasons, but primarily because the varying pathogens implicated in each category dictate the empiric therapy likely to be most useful.[3]

In children, the following conditions should also be taken into consideration:

  • Bronchiolitis

  • Croup or Laryngotracheobronchitis

  • Epiglottitis

  • Reactive Airway Disease

  • Respiratory Distress Syndrome

Differential Diagnoses

 

Workup

Approach Considerations

Diagnostic testing in patients with suspected pneumonia is driven mostly by the possibility that the results would significantly alter empiric therapy and management decisions and whether the test is likely to have a high yield.[3, 53] Diagnostic testing is also useful in classifying the severity of illness and site-of-care decisions (outpatient vs inpatient vs intensive care unit [ICU]). The most obvious indication for extensive diagnostic testing is in the critically ill patient.[3, 54]

Various tools to assess the severity of disease and risk of death exist and are in wide use, including the PSI/PORT (ie, pneumonia severity index/Patient Outcomes Research Team score), the CURB-65 system (ie, confusion, urea, respiratory rate, blood pressure, and age >65 y), and the APACHE (ie, acute physiology and chronic health evaluation), among others discussed under Risk Stratification in the Clinical Presentation section. A number of laboratory values are commonly used in the calculation of these risk indices.

Hyponatremia (sodium level < 130 mEq/L) and microhematuria may be associated with Legionella pneumonia. Sputum examination may be supplemented by using a Legionella -specific fluorescent antibody. However, this technique has a high false-negative rate.

Urinary antigen testing for Legionella serogroup 1 organisms is accurate. However, as many as 30% of infections are not caused by serogroup 1 organisms. A Legionella serum antibody titer of 1:128 or more is suggestive of the diagnosis. Pneumococcal antigen tests for serum, urine, and saliva samples have been developed. Antigen-antibody testing has little clinical effect in an emergency department setting, although it may help in recalcitrant or unclear cases.

Imaging studies are generally helpful in detecting suspected pneumonia and identifying the presence of complications. However, only occasionally do radiologic studies suggest specific pathogens.[55]

Routine Laboratory Tests

The following laboratory tests may not be useful for diagnostic purposes but are useful for classifying illness severity and site-of-care/admission decisions[38, 44, 56, 57] (see Risk Stratification under Clinical Presentation):

  • Serum chemistry panel (sodium, potassium, bicarbonate, blood urea nitrogen [BUN], creatinine, glucose)

  • Arterial blood gas (ABG) determination (serum pH, arterial oxygen saturation, arterial partial pressure of oxygen and carbon dioxide) – Hypoxia and respiratory acidosis may be present.

  • Venous blood gas determination (central venous oxygen saturation)

  • Complete blood cell (CBC) count with differential

  • Serum free cortisol value

  • Serum lactate level

A pulse oximetry finding of less than 90-92% indicates significant hypoxia, and an elevated C-reactive protein (CRP) level may be predictive of more serious disease.[58] However, CRP has not been clearly shown to differentiate bacterial versus viral illness.

Blood Studies

CBC count with differential

Leukocytosis with a left shift may be observed in any bacterial infection. However, its absence, particularly in patients who are elderly, should not cause the clinician to discount the possibility of a bacterial infection.

Leukopenia (usually defined as a WBC count < 5000 cells/µL) may be an ominous clinical sign of impending sepsis.

Coagulation studies

An elevated international normalized ratio (INR) has been associated with more severe illness. This finding may herald the development of disseminated intravascular coagulation.

Blood cultures

Blood cultures should be obtained before the administration of antibiotics. These cultures require 24 hours (minimum) to incubate. When blood cultures are positive, they correlate well with the microbiologic agent causing the pneumonia.

Unfortunately, blood cultures show poor sensitivity in pneumonia; findings are positive in approximately 40% of cases. Even in pneumococcal pneumonia, the results are often negative. Their yield may be higher in patients with more severe pneumonia/infection.

The findings probably have minimal clinical effect in treating bacterial pneumonia. Indeed, the use of blood cultures only rarely dictates a change in empiric antibiotics.

Sputum Evaluation

Sputum Gram stain and culture should be performed before initiating antibiotic therapy (if a good-quality, contaminant-sparse specimen containing < 10 squamous epithelial cells per low-power field can be obtained). The white blood cell (WBC) count should be more than 25 per low-power field in non-immunosuppressed patients.

A single predominant microbe should be noted at Gram staining. Mixed flora may be observed with anaerobic infections.

However, often, patients cannot produce an adequate specimen. Many specimens produced are so contaminated by oral materials that the results of stains and cultures are unreliable.

Cultures of the sputum have similar limitations. To be accurate, only specimens that have been examined microscopically and that have satisfied the criteria above should be submitted for culturing.

Transtracheal Aspiration

In intubated patients admitted to the ICU, some researchers suggest that airway samples for stains and cultures obtained initially on admission may aid in directing antibiotic therapy should ventilator-associated pneumonia (VAP) ensue several days after admission.[59] However, fiberoptic bronchoscopy has largely replaced transtracheal aspiration for obtaining lower respiratory secretions.

Chest Radiography

Chest radiography is considered the standard method for diagnosing the presence of pneumonia, that is, the presence of an infiltrate is required for the diagnosis. However, it must be noted that the accuracy of plain chest radiography for detecting pneumonia decreases depending on the setting of infection (see Background).

In addition, pleural effusions can be identified by chest radiographs. The presence of a parapneumonic pleural fluid can have important therapeutic implications. In H influenzae pneumonia, pleural effusion is present in approximately half of infected individuals.

Go to Imaging Typical Bacterial Pneumonia and Imaging Atypical Bacterial Pneumonia for complete information on these topics.

Lobar pneumonia

Radiographically, lobar pneumonia, or focal or nonsegmental pneumonia, is manifested as nonsegmental, homogeneous 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.

S pneumoniae infection is characterized by homogenous parenchymal lobar opacities with air bronchograms. This condition can occasionally manifest as a round opacity stimulating a pulmonary mass, called round pneumonia. Frank consolidation and air bronchograms have been associated with a higher incidence of bacteremia.

Aspiration pneumonia radiographic findings may be seen in the gravity-dependent portions of the lungs (affected by patient positioning). The classic finding is an infltrate in the right lower lobe, but aspiration pneumonia also has characteristic distributions based on patient positioning at the time of the aspiration event. The right lung is affected twice as often as the left lung. In recumbent patients, the findings are in the posterior segments of the upper lobes, and, in upright patients, the basal segments of the lower lobes are often affected.

K pneumoniae infection may show radiographic evidence of lobar expansion with bulging of interlobular fissures due to voluminous inflammatory exudate. Cavitations may also be present. Klebsiella has a tendency to occur in the upper lobes.

Legionella has a predilection for the lower lung fields. Radiologic resolution tends to lag far behind clinical improvement (eight weeks to clear).

The following radiographs depict examples of lobar pneumonia.

Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with right upper lobe pneumonia. Note the increased anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary disease (COPD).
Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with bilateral lower lobe pneumonia. Note the spine sign, or loss of progression of radiolucency of the vertebral bodies
Bacterial pneumonia. Radiographic images in a pati Bacterial pneumonia. Radiographic images in a patient with early right middle lobe pneumonia.

Bronchopneumonia

Bronchopneumonia, also known as multifocal or lobular pneumonia, 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. The 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 may develop. Pathologically, bronchopneumonia stems from inflammation of large airways (bronchitis) with patchy (lobular) involvement.

In S aureus pneumonia, lobar enlargement with bulging of interlobular fissures can be seen in severe cases. Abscesses, cavitations (with air-fluid levels), and pneumatoceles are not uncommon and 30-50% of patients develop pleural effusions, half of which are empyemas. Note that cavitation and associated pleural effusions are also observed in cases of anaerobic infections, gram-negative infections, and tuberculosis.

In P aeruginosa infection, the radiographic findings tend to be nonspecific and difficult to differentiate from underlying lung disease. Usually all the lobes are involved, with a predilection for the lower lobes, and necrosis and cavitation may occur. In addition, pulmonary vasculitis can produce areas of pulmonary infarction that radiographically resembles invasive aspergillosis.

Interstitial pneumonia

Interstitial pneumonia is 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.[60, 61]

Chest CT Scanning

The role of computed tomography (CT) scanning in the diagnosis of pneumonia is not yet well defined. For inpatients, CT scanning may identify pulmonary infections earlier than plain radiography.[54] In most cases, CT scans can be helpful in the analysis of more complex lung findings and the evaluation of other intrathoracic structures. In situations in which chest radiographs are equivocal, high-resolution CT scanning of the lungs may aid in the diagnosis.

CT patterns of disease may be broken down into abnormalities that cause either increased or decreased lung opacity.[62] Abnormalities that cause increased lung opacity include the following:

  • Nodular pattern, based on the anatomy of the secondary pulmonary lobule – A centrilobular pattern is further characterized by the presence or absence of tree-in-bud morphology, the presence of which is almost always seen in infection. Its absence is likely to expand the differential beyond infectious processes. Other nodules include perilymphatic nodules and random nodules.

  • Linear patter - Interlobular septal thickening (smooth, nodular, irregular), parenchymal bands, subpleural lines, and irregular linear opacities may be seen.

  • Reticular pattern

  • Ground-glass opacity

  • Consolidation

Abnormalities that cause decreased lung opacity include the following:

  • Bronchiectasis

  • Emphysematous change (centrilobular, panlobular, paraseptal, irregular)

  • Honeycomb lung and cystic disease

  • Mosaic perfusion and inhomogeneous lung opacity

Go to Imaging Typical Bacterial Pneumonia and Imaging Atypical Bacterial Pneumonia for complete information on these topics.

Chest Ultrasonography

Ultrasonography (US) is useful in evaluating suspected parapneumonic effusions. US can identify septations within the fluid collection that may not be visible on CT scans. US also has great utility for directing needle placement for pleural fluid aspiration (throacentesis) at the patient's bedside.[55]

BAL With and Without Bronchoscopy

Lung tissue can be visually evaluated and bronchial washing specimens can be obtained with the aid of a fiberoptic bronchoscope. Protected brushings and bronchoalveolar lavage (BAL) can be performed for fluid analysis and for stains and cultures.

BAL can also be performed without the use of a bronchoscope by insertion of a catheter into the lower respiratory tree either blindly or with fluoroscopic guidance.

Thoracentesis

Thoracentesis is an essential procedure in patients with a parapneumonic pleural effusion. Obtaining fluid from the pleural space for laboratory analysis allows for the differentiation between simple and complicated effusions. This determination may help guide further therapeutic intervention.

Biochemical analyses and cell counts should be performed on the pleural fluid. The pleural effusions and empyema fluid should also be sent for microbiologic stains and cultures.

Other Pathogen-Specific Tests

Urine assays also available for the rapid detection of Legionella and pneumococcal antigens. These fast card-type assays have been developed in recent years and may be useful in unclear cases or when the choices for antimicrobial therapy are limited.

Sputum and/or urinary antigen tests are available for Legionella pneumophila.

Sputum, serum, and/or urinary antigen tests are available for Streptococcus pneumoniae.

Immune serologic tests have been developed for Mycoplasma pneumoniae, Chlamydophila pneumoniae, L pneumophila, and Coxiella burnetii. However, the results are usually not available until several weeks after the infection, which makes these tests less useful clinically.

Nucleic acid detection (eg, polymerase chain reaction [PCR]) is still in development. PCR is extremely sensitive. The potential for false-positive results renders it less useful than other tests.

Histology

Histologic inflammatory lung changes are best described according to the pattern of infection.[2]

Lobar pneumonia

Four stages of inflammatory response are classically described, as follows:

  1. Congestion: This stage is characterized by vascular engorgement, intra-alveolar fluid, and numerous bacteria. The lung is heavy, boggy, and red.

  2. 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 liver-like consistency.

  3. Gray hepatization: This stage is characterized by progressive disintegration of red blood cells and the persistence of a fibrin exudate.

  4. 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.

Bronchopneumonia

Bronchopneumonia typically consists of foci of consolidation resulting from a suppurative, leukocyte-rich exudate that fills the bronchi, bronchioles, and adjacent alveolar spaces. In terms of gross appearance, 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 the underlying inflammation extends to the pleural surface of the lung.

 

Treatment

Approach Considerations

Almost all major decisions regarding management of pneumonia address the initial assessment of severity. See Risk Stratification under Clinical Presentation.

Perhaps the most important initial determination is that of the need for hospitalization. In determining site or level of care, options include outpatient, medical ward care, or medical intensive care unit (ICU) management.

Consider using the pneumonia severity index (PSI) score as a guide for inpatient care and mortality risk. The Agency for Healthcare Research and Quality (AHRQ) has an interactive tool to calculate the PSI score.[40]

Note that the PSI score may underestimate the patient's need for admission (ie, a young otherwise healthy patient who is vomiting or has social factors that precludes him or her taking medicine). Conversely, the PSI score tends to overestimate the mortality in the higher risk patients.

Direct admission to an intensive care unit (ICU) is mandated for any patient with septic shock requiring intravenous infusion of vasopressors to support the blood pressure or with acute respiratory failure requiring intubation and mechanical ventilation.

Patients who are severely ill and those with signs of respiratory failure, sepsis, and/or neutropenia must be stabilized before transfer. Transfer, if needed, is safe for a patient in otherwise stable condition who is being admitted for antibiotic therapy and pulmonary toilet.

Respiratory support

Antibiotic therapy is the mainstay of treatment of bacterial pneumonia. However, patients who have bronchospasm with infection benefit from inhaled bronchodilators, administered by means of a nebulizer metered-dose inhaler.

For patients with mild shortness of breath, only supplemental oxygen with a nasal cannula may be required for ventilatory support. Ventilatory support becomes necessary when supplemental oxygen is not sufficient or when the patient cannot maintain the increased work of breathing.

Moderate dyspnea requires high oxygen concentrations, such as those provided by a Venti-mask or partial rebreathing face mask. Use these masks with caution in patients with chronic obstructive pulmonary disease (COPD) and/or hypercarbia. Patients in respiratory failure or those with COPD who need high oxygen concentrations may require endotracheal intubation and ventilation.

An alternative to intubation for refractory hypoxemia may be use of continuous positive airway pressure (CPAP). Patients who are awake and can tolerate mask application may avoid intubation. However, in patients with productive cough, noninvasive ventilation is often avoided because it may impair clearance of respiratory secretions, which can lead to worsening infection and recurrent aspiration. Nasal CPAP is not usually as well tolerated as a full mask (which covers both the nose and mouth) in the emergent situation. Bi-level positive airway pressure (BiPAP) may be employed as a means of noninvasive ventilation in patients with hypercarbia.

Fluid resuscitation

Patients with hypotension and/or tachycardia may benefit from an intravenous crystalloid. Many individuals with pneumonia also have volume depletion. In elderly patients and in patients with underlying cardiac disease, care must be employed to avoid aggressive fluid administration, which may cause volume overload.

Empiric antibiotic therapy

Empiric therapy for the hospitalized patient should be initially broad and cover the likely causative organisms. Use caution in patients who are elderly or debilitated. If bacteremia is present in persons with pneumococcus who are older than 80 years, the mortality rate remains approximately 40%, even with aggressive treatment.

Many regions have guidelines for evaluation and treatment of community-acquired pneumonia (CAP). This usually includes a maximum time from door to antibiotic administration of four hours or less. Failure to abide by these time parameters may be associated with poor outcome. When in doubt, administer the first antibiotic dose.

Other initial treatments may include correction of electrolyte levels and chest physiotherapy (to assist in drainage of secretions).

See Antimicrobial Therapy.

Corticosteroids

The role of supplementing corticosteroids in patients with hypotension from septic shock remains controversial. Previously, it was recommended that septic patients who were hypotensive despite fluid resuscitation and vasopressor support be screened for occult adrenal insufficiency. However, current guidelines recommend empiric therapy with stress-dose steroids in these patients who remain hypotensive despite fluids and pressors, to avoid delay in treatment of presumed adrenal insufficiency.[63]

The role of corticosteroids in patients hospitalized for CAP was evaluated in a 2015 meta-analysis of 13 randomized controlled trials, which found with high certainty that systemic corticosteroid steroid treatment reduced the duration of hospitalization by approximately 1 day and had a 5% absolute reduction in risk for mechanical ventilation.[64] The study also found that patients with severe pneumonia who received systemic corticosteroids had an apparent mortality benefit over patients with severe pneumonia who did not receive systemic corticosteroids, which may be related to the higher incidence of acute respiratory distress syndrome and the need for mechanical ventilation in patients with severe pneumonia. However, this evidence was rated moderate as the confidence interval crossed 1 and because of a possible subgroup effect. All patients who received corticosteroids had a higher incidence of hyperglycemia requiring treatment in this study. Thus, in immunocompetent patients hospitalized with severe CAP, systemic corticosteroids should be considered given the possible mortality benefit of systemic corticosteroid treatment in this subgroup of patients.

Drotrecogin alfa

A recombinant version of human activated protein C, drotrecogin alfa (Xigris), was withdrawn from the worldwide market in 2011 after it failed to demonstrate a statistically significant reduction in 28-day all-cause mortality in patients with severe sepsis and septic shock.

Antimicrobial Therapy for Bacterial Pneumonia

The goals of pharmacotherapy for bacteria pneumonia are to eradicate the infection, reduce morbidity, and prevent complications.

Treatment of pneumonia depends largely on the empiric use of antibiotic regimens directed against potential pathogens as determined by the setting in which the infection took place and the potential for exposure to multidrug-resistant (MDR) organisms and other more virulent pathogens (ie, community-acquired pneumonia [CAP], healthcare-acquired pneumonia [HCAP], hospital-acquired pneumonia [HAP], ventilator-associated pneumonia [VAP]). Discussion of empiric antibiotic therapy should be based on hospitalization status.

The information in this section is derived mainly from the current Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) guidelines for the management of CAP.[3] These guidelines have been assessed in research studies since their release, with evidence of improved health outcomes, decreased length of hospital stay, and overall decreased mortality in patients hospitalized with CAP.[65, 66]

As discussed earlier, initial empiric therapy for hospitalized patients should be broad and cover the likely causative organisms. Direct the use of antibiotic agents in bacterial pneumonia based on laboratory data as well as clinical response.

The possibility of Legionella infection should always be considered when evaluating CAP, because delayed treatment significantly increases mortality. The most prevalent causative organism is S pneumoniae, regardless of the host or the setting. Empiric antibiotic therapy must be selected with this micro-organism in mind.

Antibiotics and HAP and VAP

The prevalence and resistance patterns of MDR pathogens vary between institutions and even between ICUs within the same institution. Therefore, appropriate initial antibiotic therapy for HAP and VAP may vary markedly according to hospital site. Antimicrobial prescribing practices should not necessarily be based on national guidelines, but rather on patterns of MDR organisms at individual institutions.[8]

The table below presents first- and second-line antibiotic choices for specific organisms that cause bacterial pneumonia.

Table. Pathogen-Driven Antibiotic Choices [3] (Open Table in a new window)

Organism

First-Line Antimicrobials

Alternative Antimicrobials

Streptococcus pneumoniae

 

Penicillin susceptible

(MIC < 2 mcg/mL)

Penicillin G, amoxicillin

Macrolide, cephalosporin (oral or parenteral), clindamycin, doxycycline, respiratory fluoroquinolone

 

Penicillin resistant

(MIC ≥2 mcg/mL)

Agents chosen on the basis of sensitivity

Vancomycin, linezolid, high-dose amoxicillin (3 g/d with MIC ≤4 mcg/mL

Staphylococcus aureus

 

Methicillin susceptible

Antistaphylococcal penicillin

Cefazolin, clindamycin

 

Methicillin resistant

Vancomycin, linezolid

Trimethoprim- sulfamethoxazole

Haemophilus influenzae

 

Non–beta-lactamase producing

Amoxicillin

Fluoroquinolone, doxycycline, azithromycin, clarithromycin

 

Beta-lactamase producing

Second- or third-generation cephalosporin, amoxicillin/clavulanate

Fluoroquinolone, doxycycline, azithromycin, clarithromycin

Mycoplasma pneumoniae

Macrolide, tetracycline

Fluoroquinolone

Chlamydophila pneumoniae

Macrolide, tetracycline

Fluoroquinolone

Legionella species

Fluoroquinolone, azithromycin

Doxycycline

Chlamydophila psittaci

Tetracycline

Macrolide

Coxiella burnetii

Tetracycline

Macrolide

Francisella tularensis

Doxycycline

Gentamicin, streptomycin

Yersinia pestis

Streptomycin, gentamicin

Doxycycline, fluoroquinolone

Bacillus anthracis (inhalational)

Ciprofloxacin, levofloxacin, doxycycline

Other fluoroquinolones, beta-lactam (if susceptible), rifampin, clindamycin, chloramphenicol

Enterobacteriaceae

Third-generation cephalosporin, carbapenem

Beta-lactam/beta-lactamase inhibitor, fluoroquinolone

Pseudomonas aeruginosa

Antipseudomonal beta-lactam plus ciprofloxacin, levofloxacin, or aminoglycoside

Aminoglycoside plus ciprofloxacin or levofloxacin

Bordetella pertussis

Macrolide

Trimethoprim- sulfamethoxazole

Anaerobe (aspiration)

Beta-lactam/beta-lactamase inhibitor, clindamycin

Carbapenem

MIC = Minimal inhibitory concentration.

Outpatient Empiric Antibiotic Therapy

Antibiotic choices in the outpatient setting should be driven by the presence of patient risk factors, including recent exposure to antibiotics, comorbidities, and local trends in antibiotic resistance.

In previously healthy patients with no exposure to antibiotics within the previous 90 days, use a macrolide or doxycycline (weak recommendation).

In patients with comorbidities such as chronic disease of the heart, lung, liver, or kidneys, diabetes mellitus, alcoholism, malignancy, immunosuppression (drug- or disease-induced), or use of antimicrobials within the last 90 days, use a respiratory fluoroquinolone or beta-lactam plus a macrolide.

If the patient was exposed to antibiotics within the previous 90 days for systemic treatment of any type of bacterial infection, an alternative agent from a different class should be selected for treatment of the current illness.

Inpatient Empiric Antibiotic Therapy

According to the 2009 Centers for Medicare and Medicaid Services (CMS) and Joint Commission consensus guidelines, inpatient treatment of pneumonia should be given within four hours of hospital admission (or in the emergency department if this is where the patient initially presented) and should consist of the following antibiotic regimens,[67] which are also in accordance with IDSA/ATS guidelines.[3]

For non-intensive care unit (ICU) patients, choose one option below:

  • Beta-lactam (intravenous [IV] or intramuscular [IM] administration) plus macrolide (IV or oral [PO])

  • Beta-lactam (IV or IM) plus doxycycline (IV or PO)

  • Antipneumococcal quinolone monotherapy (IV or IM)

  • If the patient is younger than 65 years with no risk factors for drug-resistant organisms, administer macrolide monotherapy (IV or PO)

For ICU patients, choose one option below:

  • IV beta-lactam plus IV macrolide

  • IV beta-lactam plus IV antipneumococcal quinolone

  • If the patient has a documented beta-lactam allergy, administer IV antipneumococcal quinolone plus IV aztreonam

For patients at increased risk of infection with Pseudomonas (acceptable for both ICU and non-ICU patients), choose one option below:

  • IV antipseudomonal beta-lactam plus IV antipseudomonal quinolone (PO quinolone in non-ICU patients only)

  • IV antipseudomonal beta-lactam plus IV aminoglycoside plus one of the following: (1) IV macrolide; (2) IV antipneumococcal quinolone (PO in non-ICU patients only); or (3) if the patient has a documented beta-lactam allergy, administer IV aztreonam plus IV aminoglycoside plus IV antipneumococcal quinolone (PO quinolone in non-ICU only)

  • The question of the need for “double coverage” for possible drug-resistant pseudomonal organisms often arises when treating critically ill patients. The use of two antipseudomonal medications should only be considered in critically ill patients who are at high risk for infection with drug-resistant organisms. Double coverage should be given as initial therapy early in the course of treatment in order to make an impact in the disease course.

Aspiration Pneumonia Empiric Therapy

Patients with severe periodontal disease, putrid sputum, or a history of alcoholism with suspected aspiration pneumonia may be at greater risk of anaerobic infection. One of the following antibiotic regimens is suggested for such patients[3, 17] :

  • Piperacillin-tazobactam

  • Imipenem

  • Clindamycin or metronidazole plus a respiratory fluoroquinolone plus ceftriaxone

MRSA empiric antibiotic therapy

For suspected infection with methicillin-resistant S aureus (MRSA), vancomycin or linezolid may be added to the antibiotic regimen until the organism's identity and antibiotic sensitivities are known, at which point the medications can be adjusted accordingly. Note, however, that when nine studies were combined in a meta-analysis, linezolid was not superior in terms of higher cure rates for MRSA pneumonia when compared with the glycopeptides vancomycin and teicoplanin.[68] In addition, neither vancomycin nor linezolid is an optimal agent for the treatment of methicillin-sensitive S aureus (MSSA).[3]

Other agents that may be considered for use against MRSA include clindamycin, trimethoprim-sulfamethoxazole (TMP-SMZ), gentamicin, ciprofloxacin, and rifampin. More antibiotics are being evaluated for activity against MRSA.[69]

Bacterial pneumonia and viral infection

The influenza pandemic of 1918 was responsible for the deaths of approximately 40-50 million people worldwide (>600,000 deaths in the United States). Many of the deaths were likely due to secondary bacterial infection.[22]

With the 2009 H1N1 influenza A pandemic, the US Centers for Disease Control and Prevention (CDC) mortality estimates ranged from 8,800 to 18,000 between April 2009 and April 2010. Similar to 1918, the vast majority of deaths occurred in individuals younger than 65 years.[70] Evaluation of 77 postmortem lung specimens by the CDC revealed that 29% of those that died also had evidence of bacterial coinfection.[71]

Such statistics highlight the importance of the prevention of influenza spread with vaccination and treatment with antiviral drugs as well as place focus on the diagnosis of, treatment of, and prophylaxis against bacterial pathogens with appropriate antibiotics and the pneumococcal vaccination.[22]

Supportive Measures

Supportive measures include the following (some were mentioned previously):

  • Analgesia and antipyretics

  • Chest physiotherapy

  • Intravenous fluids (and, conversely, diuretics) if indicated

  • Monitoring – Pulse oximetry with or without cardiac monitoring, as indicated

  • Oxygen supplementation

  • Positioning of the patient to minimize aspiration risk

  • Respiratory therapy, including treatment with bronchodilators and, perhaps, N -acetylcysteine in selected patients

  • Suctioning and bronchial hygiene – Pulmonary toilet may include active suction of secretions, chest physiotherapy, positioning to promote dependent drainage, and incentive spirometry to enhance elimination of purulent sputum and to avoid atelectasis.

  • Mechanical ventilatory support with low tidal volumes (6 mL/kg of ideal body weight) in patients with respiratory failure secondary to bilateral pneumonia or acute respiratory distress syndrome (ARDS)[3]

  • Systemic support may include proper hydration, nutrition, and early mobilization to create a positive host milieu to fight infection and speed recovery. Early mobilization of patients, with encouragement to sit, stand, and walk when tolerated, speeds recovery.

Clinical Resolution

Clinical response to antibiotic therapy should be evaluated within 48-72 hours of initiation. With appropriate antibiotic therapy, improvement in the clinical manifestations of pneumonia should be observed in 48-72 hours. Because of the time required for antibiotics to act, antibiotics should not be changed within the first 72 hours unless marked clinical deterioration occurs or the causative micro-organism is identified with some certainty. With pneumococcal pneumonia, the cough usually resolves within eight days and crackles heard on auscultation clear within three weeks.

The timing of radiologic resolution of pneumococcal pneumonia varies with patient age, the severity of the pneumonia, and the presence or absence of an underlying lung disease. The chest radiograph usually clears within four weeks in patients younger than 50 years without underlying pulmonary disease. In contrast, resolution may be delayed for 12 weeks or longer in older individuals and those with underlying lung disease.

Pneumonia that does not respond to treatment poses a clinical dilemma and is a common concern. If patients do not improve within 72 hours, an organism that is not susceptible or is resistant to the initial empiric antibiotic regimen should be considered. Lack of response may also be secondary to a complication such as empyema or abscess formation.

Also consider broadening the differential diagnosis to include noninfectious etiologies such as malignancies, inflammatory conditions, or congestive heart failure. In patients in whom the precipitating factor is airway obstruction by a neoplasm or a foreign body, the post-obstructive infiltrate may fail to clear. Computed tomography (CT) scanning may be helpful in unclear cases and in delineating more complex pulmonary processes. Carefully review the patient's medical history, especially in regard to potential inhaled respiratory exposure. See Diagnosis.

Diagnostic testing may require more complex studies when the cause of disease is less apparent. Unresponsive cases of pneumonia may require fiberoptic bronchoscopy or open lung biopsy for definitive diagnosis. Bronchoscopy helps evaluate for airway obstruction due to a foreign body or neoplasm. Transbronchial biopsy may be helpful in some cases. Lung biopsy may need to be performed if all other procedures do not establish a diagnosis and the illness continues. The lung biopsy may be performed under CT guidance, by thoracoscopy, or with open thoracotomy. See Workup.

Prevention

Vaccination and other prevention guidelines are briefly discussed below.

Pneumococcal vaccine recommendations

In 2015, the Advisory Committee on Immunization Practices provided recommendations on the pneumococcal polysaccharide vaccine (PPSV23) and the pneumococcal conjugate vaccine (PCV13), summarized as follows[72, 73] :

  • For immunocompetent adults aged  65 years and older who have not previously received pneumococcal vaccine, the Advisory Committee on Immunization Practices (ACIP) makes the following recommendation for intervals between pneumococcal conjugate vaccine (PCV13) followed by pneumococcal polysaccharide vaccine (PPSV23): A dose of PPSV23 should be given 1 year or more following a dose of PCV13. The 2 vaccines should not be co-administered. If a dose of PPSV23 is inadvertently given earlier than the recommended interval, the dose need not be repeated.
  • The ACIP currently recommends that a dose of PCV13 be followed by a dose of PPSV23 in persons aged 2 years or older who are at high risk for pneumococcal disease because of underlying medical conditions.
  • Children with an immunocompromising condition or functional or anatomic asplenia should receive a second dose of PPSV23 5 years after the first PPSV23 dose.

See Vaccinations - Adult and Vaccinations - Infants and Children for more information.

Prevention of community-acquired pneumonia

Administration of influenza vaccine decreases fall and/or winter risk of viral influenza, which decreases the risk of bacterial superinfection. This vaccine is especially important in patients who are elderly and in those with comorbid illnesses. In fact, influenza vaccination for elderly individuals results in a 48-57% reduction of the rate of hospitalization for pneumonia and influenza.

Although pneumococcal vaccines are effective, they are unfortunately underused. Streptococcus pneumoniae is the most common cause of fatal pneumonia and pneumonia overall. The incidence of pneumococcal disease is the highest in children younger than two years and in adults older than 65 years. Other important risk factors for pneumococcal pneumonia are chronic heart disease, chronic lung disease, cigarette smoking, and asplenia.

A 23-valent capsular polysaccharide vaccine (Pneumovax 23) and a 13-valent protein-polysaccharide conjugate vaccine (Prevnar 13) are currently available in the United States. Both vaccines are efficacious in the prevention of invasive pneumococcal disease. The role of the pneumococcal vaccine has not been defined as clearly as that of the influenza vaccine in adults. Pneumococcal 13-valent conjugate vaccine is approved for children aged six weeks to five years and adults aged 50 years or older. The pneumococcal 23-valent vaccine is approved for adults aged 50 years or older and persons aged two years or older who are at increased risk for pneumococcal disease.

On October 12, 2012, the Advisory Committee on Immunization Practices (ACIP) published updated recommendations for pneumococcal vaccination of high-risk adults. The committee recommends routine use of Prevnar 13 in addition to the previously recommended Pneumovax 23 for adults aged 19 years and older with immunocompromising conditions (eg, HIV, cancer, renal disease), functional or anatomic asplenia, cerebrospinal fluid leaks, or cochlear implants. Patients who have not previously received either vaccine should be given one dose of Prevnar 13 followed by one dose of Pneumovax 23 after at least eight weeks. In patients who have previously received Pneumovax 23 vaccine, administer one dose of Prevnar 13 at least one year after the last Pneumovax 23 dose.[74]

On August 13, 2014, the CDC’s Advisory Committee on Immunization Practices (ACIP) recommended routine use of pneumococcal vaccine 13-valent (PCV13 [Prevnar 13]) among adults aged 65 years and older.[75] PCV13 should be administered in series with the 23-valent pneumococcal vaccine polyvalent (PPSV23 [Pneumovax23]), the vaccine currently recommended for adults aged 65 years and older. PCV13 was approved by the Food and Drug Administration (FDA) in late 2011 for use among adults aged 50 years and older. In June 2014, the results of a randomized placebo-controlled trial evaluating efficacy of PCV13 for preventing community-acquired pneumonia among approximately 85,000 adults aged 65 years and older with no prior pneumococcal vaccination history (CAPiTA trial) became available and were presented to ACIP.[76]

It is also important to emphasize smoking cessation to all patients but particularly those at risk of pneumonia and influenza.

Go to Community-Acquired Pneumonia for complete information on this topic.

Prevention of nosocomial pneumonia

A number of preventative strategies have been applied in the prevention of nosocomial pneumonia. Some of these probably are effective or promising, and some are currently being evaluated.

The efficacious regimens are hand washing and isolation of patients with multiple resistant respiratory tract pathogens. Hand washing between patient contacts is a basic and often neglected behavior by medical personnel.

Interventions that should be considered or undertaken include nutritional support, attention to the size and nature of the gastrointestinal reservoir of microorganisms, careful handling of ventilator tubing and associated equipment, subglottic secretion drainage, and lateral-rotation bed therapy.

Go to Nosocomial Pneumonia for complete information on this topic.

Consultations

Consultation with infectious disease and/or pulmonary specialists is suggested in difficult cases. In addition, a pharmacist and/or infection control specialist may be of assistance in providing information on hospital or regional bacterial resistance and sensitivity patterns and in appropriate antibiotic dosing and level monitoring.

Patients requiring noninvasive mechanical ventilation or intubation may need consultation with a critical care medicine specialist to aid in management after admission to the intensive care unit (ICU).

Long-Term Monitoring

When a patient with bacterial pneumonia is treated in an outpatient setting, arranging adequate follow-up evaluations is mandatory. The patient should also be instructed to return promptly if their condition deteriorates.

Patients should have a follow-up chest radiograph in approximately six weeks to ensure resolution of the consolidation and to assess persistent abnormality of the lung parenchyma (eg, scarring, bronchiectasis). Chest radiograph findings indicating nonresolution of the infiltrate should raise the consideration of an endobronchial obstruction as a cause of postobstructive pneumonia or a pleural effusion. Computed tomograph (CT) scanning may be of benefit in these cases.

Although guidelines have routinely recommended follow-up chest radiography in order to exclude underlying lung cancer, studies have found that the incidence of lung cancer following pneumonia is relatively low. One study suggested that age 50 years and older, male sex, and smoking are the only patient characteristics that were independently associated with a new lung cancer diagnosis.[77]

 

Medication

Medication Summary

The mainstay of drug therapy for bacterial pneumonia is antibiotic treatment. The choice of agent is based on the severity of the patient's illness, host factors (eg, comorbidity, age), and the presumed causative agent. Although intravenous (IV) penicillin G is currently not favored, doses in the range of 20-24 million U/d result in serum levels that exceed minimum inhibitory concentration (MIC) levels of most resistant pneumococci.

Glucocorticoids

The role of glucocorticoids in acute bacterial pneumonia has yet to be clearly elucidated. Classic teaching warns that the use of glucocorticoids in infection may impair the immune response. However, findings demonstrate that local pulmonary inflammation may be reduced with systemic glucocorticoids. In a 2015 meta-analysis of 13 randomized controlled trials evaluating the use of systemic corticosteroids in patients hospitalized for CAP,[64] it was found with high certainty that systemic corticosteroid steroid treatment reduced the duration of hospitalization by approximately 1 day and had a 5% absolute reduction in risk for mechanical ventilation. The study also found that patients with severe pneumonia who received systemic corticosteroids had an apparent mortality benefit over patients with severe pneumonia who did not receive systemic corticosteroids, which may be related to the higher incidence of acute respiratory distress syndrome and the need for mechanical ventilation in patients with severe pneumonia. However, this evidence was rated moderate as the confidence interval crossed 1 and because of a possible subgroup effect. All patients who received corticosteroids had a higher incidence of hyperglycemia requiring treatment. Thus, in immunocompetent patients hospitalized with severe CAP, systemic corticosteroids should be considered, given the possible mortality benefit of systemic corticosteroid treatment in this subgroup of patients.

Outpatient/inpatient antibiotic administration

Outpatients are typically treated with oral antibiotics. For the most part, parenteral medications are given to patients admitted to the hospital. This rationale does not preclude the clinician from giving an initial intravenous (IV) dose of antibiotics in the emergency department and then sending the patient home on oral agents, if the patient's condition warrants this action. The patient's condition, infection severity, and microorganism susceptibility should determine the proper dose and route of administration.

A rational approach may be to administer an oral extended-spectrum macrolide or amoxicillin and clavulanate (Augmentin) to those with mild, outpatient disease. Oral fluoroquinolone may be substituted if a comorbid illness or allergy to the first-line agents is present or for good dosing compliance. Admitted patients should receive IV therapy, a third-generation cephalosporin alone or with a macrolide. An alternative regimen would be IV fluoroquinolones alone.

Pediatric antimicrobial therapy

All agents discussed in the next sections are for use in persons older than 5 years. In children younger than five years of age, initial treatment of pneumonia includes IV ampicillin or nafcillin plus gentamicin or cefotaxime (for neonates). Ceftriaxone or cefotaxime can be administered as a single agent (for >28 d to 5 y). An alternative regimen includes a penicillinase-resistant penicillin plus an antipseudomonal aminoglycoside.

Outpatient treatment of mild-to-moderate pneumonias in children usually involves agents similar to those used for acute otitis media. Most of the pneumonias in these patients probably have a viral cause. In children who have features suggesting a bacterial etiology (eg, an infiltrate on chest radiograph and/or positive findings at sputum Gram stain), the administration of antibiotics may be good clinical practice. In these cases, many clinicians begin empiric therapy with amoxicillin, but its spectrum of activity is lacking, because children in this group who do not have nonviral pneumonia usually have an infection caused by S pneumoniae and Mycoplasma species.

H influenzae type B has been less common since the introduction of the HIB vaccine. Children younger than two years may still be at risk for H influenzae type B infection, because their immune response is not sufficient, as it is in older children. A typical regimen for outpatient therapy may include a new macrolide agent or a second-generation or third-generation cephalosporin. Cost is a potential drawback for all agents.

Macrolides

The best initial antibiotic choice is thought to be a macrolide. Macrolides provide the best coverage for the most likely organisms in community-acquired bacterial pneumonia (CAP). Macrolides have effective coverage for gram-positive, Legionella, and Mycoplasma organisms. Azithromycin administered intravenously is an alternative to intravenous erythromycin.

Macrolides, as a class, have the potential disadvantage of causing gastrointestinal (GI) upset. Compared with erythromycin, newer agents have fewer GI adverse effects and drug interactions, although all macrolides have the potential for drug interactions similar to those of erythromycin. Newer macrolides offer improved compliance because of reduced dosing frequency, improved action against H influenzae, and coverage of Mycoplasma species (unlike cephalosporins). The main disadvantage is cost.

Macrolides are primarily recommended for the treatment of CAP in patients younger than 60 years of age who are nonsmokers without a comorbid illness. Give special consideration to recommendations for antibiotic use in patients with comorbid illnesses or those with CAP who are older than 60 years of age. Although patients in this group are still susceptible to S pneumoniae, they should receive treatment for broader coverage that includes Haemophilus, Moraxella, and other gram-negative organisms. Therefore, a prudent course of action for empiric outpatient therapy is to include: (1) one of the macrolide agents described previously plus a second- or third-generation cephalosporin or amoxicillin and clavulanate or (2) trimethoprim and sulfamethoxazole (TMP-SMZ) as a single agent.

Patients who have moderate clinical impairment or comorbid illnesses are best treated with parenteral agents and, unless a particular agent is strongly suspected, broad coverage should be afforded. Regimens for this use include a macrolide plus a second- or third-generation cephalosporin, (as single agents) ampicillin and sulbactam (Unasyn), piperacillin and tazobactam (Zosyn), or ticarcillin and clavulanate (Timentin).

Cephalosporins

Second-generation cephalosporins maintain the gram-positive activity of first-generation cephalosporins, provide good coverage against Proteus mirabilis, H influenzae, E coli, K pneumoniae, and Moraxella species, and provide adequate activity against gram-positive organisms.

Of these agents, cefprozil, cefpodoxime, and cefuroxime seem to have better in vitro activity against S pneumoniae. Second-generation cephalosporins are not effective against Legionella or Mycoplasma species. These drugs are generally well tolerated, but cost may be a factor. Oral second-generation and third-generation cephalosporins offer increased activity against gram-negative agents and may be effective against ampicillin-resistant S pneumoniae.

Third-generation cephalosporins have wider activity against most gram-negative bacteria (eg, Enterobacter, Citrobacter, Serratia, Neisseria, Providencia, Haemophilus species), including beta-lactamase–producing strains.

Intravenous cephalosporins may be combined with a macrolide agent. They broaden the gram-negative coverage, and in the case of third-generation agents, they may be effective against resistant S pneumoniae. In addition, some third-generation agents are effective against Pseudomonas, whereas second-generation agents are not.

Combination drugs

The combination of trimethoprim and sulfamethoxazole (TMP-SMZ) may be used in the patient with pneumonia and a history of chronic obstructive pulmonary disease (COPD) or smoking. It may be also used as a single agent in younger patients in whom a Haemophilus species is the suspected agent.

TMP-SMZ is well tolerated and inexpensive. However, allergic reactions are more often associated with drugs in this class than with other antibiotics. Reactions span the spectrum from simple rash (most likely) to Steven-Johnson syndrome and toxic epidermal necrolysis (rare). Many potential drug interactions are noted.

When a severely ill patient has features of sepsis and/or respiratory failure, and/or when neutropenia is known or suspected, treatment with an intravenous macrolide is combined with an intravenous third-generation cephalosporin and vancomycin. An alternative regimen may include imipenem, meropenem, or piperacillin and tazobactam plus a macrolide and vancomycin. A fulminant course also must raise the suspicion of infection with Legionella or Mycoplasma species, Hantavirus, psittacosis, or Q fever.

Fluoroquinolones, including levofloxacin, moxifloxacin, and gatifloxacin, may also be used. These agents are available in oral and parenteral forms and have convenient dosing regimens, which allow easier conversion to oral therapy that results in good patient compliance. Note that in July 2008, a warning was issued from the US Food and Drug Administration (FDA) regarding the risk of tendonitis and tendon rupture with fluoroquinolone use.[78]

Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Azithromycin (Zithromax)

In otherwise uncomplicated pneumonia, azithromycin is the initial drug of choice, as it covers most of the potential etiologic agents, including Mycoplasma species. Compared with other drugs, this agent also causes less GI upset, and it has the potential for good compliance because of its reduced dosing frequency. Azithromycin has better action against H influenzae compared with erythromycin, but its main disadvantage is cost.

Azithromycin is a macrolide that acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected. This agent concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that the concentration in phagocytes may contribute to drug distribution to inflamed tissues.

Aztreonam (Azactam)

Aztreonam is a monobactam, not a beta-lactam, antibiotic that inhibits cell wall synthesis during bacterial growth. This agent has activity against gram-negative bacilli but very limited gram-positive activity, and it is not useful for anaerobes. Aztreonam lacks cross-sensitivity with beta-lactam antibiotics; it may be used in patients allergic to penicillins or cephalosporins.

The duration of aztreonam therapy depends on the severity of the infection and is continued for at least 48 hours after the patient is asymptomatic or evidence of bacterial eradication is obtained. Doses smaller than indicated should not be used.

Transient or persistent renal insufficiency may prolong serum levels. After an initial loading dose of 1 or 2 g, reduce the dose by half for an estimated creatinine clearance (CrCl) rate of 10-30 mL/min/1.73 m2. When only serum creatinine concentration is available, the following formula (based on sex, weight, and age) can approximate CrCl. Serum creatinine should represent a steady state of renal function.

Males: CrCl = [(weight in kg)(140 - age)] divided by (72 X serum creatinine in mg/dL)

Females: 0.85 X above value

In patients with severe renal failure (CrCl < 10 mL/min/1.73 m2) and those supported by hemodialysis, a usual dose of 500 mg, 1 g, or 2 g, is given initially.

The maintenance dose is one fourth of the usual initial dose given at a usual fixed interval of 6, 8, or 12 hours.

For serious or life-threatening infections, supplement the maintenance doses with one eighth of the initial dose after each hemodialysis session.

Elderly persons may have diminished renal function. Renal status is a major determinant of dosage in these patients. Serum creatinine may not be an accurate determinant of renal status. Therefore, as with all antibiotics eliminated by the kidneys, obtain estimates of the CrCl, and make appropriate dosage modifications. Data are insufficient regarding intramuscular (IM) administration to pediatric patients or dosing in pediatric patients with renal impairment. Aztreonam is administered IV only to pediatric patients with normal renal function.

Cefepime (Maxipime)

Cefepime is the best beta-lactam for IM administration. This agent is a fourth-generation cephalosporin that has gram-negative coverage comparable to ceftazidime but with better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion, so it rapidly penetrates gram-negative cells. However, this agent has a poor capacity to cross the blood-brain barrier, which precludes its use for the treatment of meningitis.

Cefotaxime (Claforan)

Cefotaxime is a third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. It acts by arresting bacterial cell wall synthesis by binding to one or more penicillin-binding proteins, which, in turn, inhibits bacterial growth. Cefotaxime is used for septicemia and treatment of gynecologic infections caused by susceptible organisms, but it has a lower efficacy against gram-positive organisms.

Cefuroxime (Ceftin, Kefurox, Zinacef)

Cefuroxime is a second-generation cephalosporin that maintains gram-positive activity of first-generation cephalosporins, as well as adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis. This agent binds to penicillin-binding proteins and inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death.

The condition of patient, severity of infection, and susceptibility of microorganism determine the proper dose and route of administration. Cefuroxime resists degradation by beta-lactamase.

Ciprofloxacin (Cipro)

Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for the replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms but no activity against anaerobes. Continue ciprofloxacin treatment for at least 2 days (7-14 d typical) after the patient's signs and symptoms have disappeared.

Clindamycin (Cleocin)

Clindamycin is a lincosamide semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of the parent compound lincomycin. This agent inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Clindamycin widely distributes in the body without penetration of the central nervous system (CNS). It is protein bound and excreted by liver and kidneys.

Clindamycin is available in parenteral (ie, clindamycin phosphate) and oral form (ie, clindamycin hydrochloride). Oral clindamycin is absorbed rapidly and almost completely and is not appreciably altered by presence of food in stomach. Appropriate serum levels are reached and sustained for at least 6 hours following the oral dose. No significant levels are attained in the cerebrospinal fluid (CSF). Clindamycin is also effective against aerobic and anaerobic streptococci (except enterococci).

Doxycycline (Bio-Tab, Doryx, Doxy, Periostat, Vibramycin, Vibra-Tabs)

Doxycycline is an alternative agent for patients who cannot tolerate macrolides or penicillins. This agent is a broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. Doxycycline is almost completely absorbed, concentrates in the bile, and is excreted in urine and feces as a biologically active metabolite in high concentrations.

Doxycycline inhibits protein synthesis and, thus, bacterial growth, by binding to the 30S and possibly 50S ribosomal subunits of susceptible bacteria. It may block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Ertapenem (Invanz)

Ertapenem is indicated for community-acquired pneumonia due to S pneumoniae (penicillin-susceptible isolates only) including cases with concurrent bacteremia, H influenzae (beta-lactamase negative isolates only), or M catarrhalis.

This agent is a carbapenem antibiotic that has bactericidal activity resulting from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Ertapenem is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. It is hydrolyzed by metallo-beta-lactamases.

Linezolid (Zyvox)

Linezolid is used as an alternative drug in patients allergic to vancomycin and for treatment of vancomycin-resistant enterococci. It is also effective against MRSA and penicillin-susceptible S pneumoniae infections.

This agent is an oxazolidinone antibiotic that prevents formation of the functional 70S initiation complex, which is essential for bacterial translation process. Linezolid is bacteriostatic against enterococci and staphylococci and bactericidal against most strains of streptococci.

The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[72]

Gentamicin (Gentacidin)

Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. This drug is used in combination with both an agent against gram-positive organisms and one that covers anaerobes.

Note that gentamicin is not the drug of choice. Consider using this drug if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms. The dosing regimens are numerous. Adjust the dose based on CrCl and changes in volume of distribution. Gentamicin may be administered IV/IM.

Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Cotrim, Cotrim DS, Septra, Septra DS)

Sulfamethoxazole and trimethoprim is a sulfonamide derivative antibiotic. This agent inhibits bacterial synthesis of dihydrofolic acid by competing with paraaminobenzoic acid, thereby inhibiting folic acid synthesis and resulting in inhibition of bacterial growth. The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except P aeruginosa.

Amoxicillin and clavulanate (Augmentin, Augmentin XR)

Amoxicillin and clavulanate is an alternative agent for patients who are allergic or intolerant to macrolides. Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. The addition of clavulanate inhibits beta-lactamase producing bacteria.

This drug combination is usually well tolerated and provides good coverage to most infectious agents. However, it is not effective against Mycoplasma and Legionella species. The half-life of the oral dosage form is 1-1.3 hours, and it has good tissue penetration but does not enter the cerebrospinal fluid.

For children older than 3 months, base the dosing protocol on the amoxicillin content. Owing to different amoxicillin/clavulanic acid ratios in the 250-mg tablet (250/125) vs 250-mg chewable tablet (250/62.5), do not use the 250-mg tablet until the child weighs >40 kg.

Cost is a problem.

Ampicillin and sulbactam (Unasyn)

This drug is a combination of beta-lactamase inhibitor with ampicillin that is used as an alternative to amoxicillin when the patient unable to take oral medication. Ampicillin and sulbactam covers skin flora, enteric flora, and anaerobes, but it is not ideal for nosocomial pathogens. It interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms.

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

Ceftazidime is a third-generation cephalosporin with broad-spectrum, gram-negative activity, including Pseudomonas; low efficacy against gram-positive organisms; and high efficacy against resistant organisms. This agent arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis.

The condition of the patient, severity of infection, and susceptibility of the microorganism should determine the proper dose and route of administration.

Ceftazidime/avibactam (Avycaz)

This combination is indicated for hospital-acquired and ventilator-associated bacterial pneumonia (HABP/VABP) caused by the following susceptible Gram-negative microorganisms: Klebsiella pneumoniae, Enterobacter cloacae, Escherichia coli, Serratia marcescens, Proteus mirabilis, Pseudomonas aeruginosa, and Haemophilus influenzae in patients aged 18 years or older.

Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity; low efficacy against gram-positive organisms; and high efficacy against resistant organisms. It is considered the drug of choice for parenteral agents in community-acquired pneumonia. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin binding proteins. This agent exerts its antimicrobial effect by interfering with the synthesis of peptidoglycan, a major structural component of the bacterial cell wall. Bacteria eventually lyse due to ongoing activity of cell wall autolytic enzymes while the cell wall assembly is arrested.

Ceftriaxone is highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, and of gram-negative and gram-positive bacteria. Approximately 33-67% of the dose excreted unchanged in urine, and the remainder is secreted in bile and, ultimately, in feces as microbiologically inactive compounds. This agent reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations of less than 25 mcg/mL to 85% bound at 300 mcg/mL.

Amoxicillin (Amoxil, Biomox, Trimox)

Amoxicillin is a penicillin derivative of ampicillin with a similar antibacterial spectrum, namely certain gram-positive and gram-negative organisms. This agent has superior bioavailability and stability to gastric acid and has a broader spectrum of activity than penicillin. However, amoxicillin is somewhat less active than penicillin against S pneumococcus. Penicillin-resistant strains are also resistant to amoxicillin, but higher doses may be effective. Amoxicillin is more effective against gram-negative organisms (eg, N meningitidis, H influenzae) than penicillin.

This agent interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Imipenem and cilastatin (Primaxin)

Imipenem and cilastatin is a carbapenem antibiotic used for treatment of multiple organism infections in which other agents do not have wide spectrum coverage or are contraindicated due to the potential for toxicity. Use this agent with caution in the presence of renal insufficiency (adjust the dose), a history of seizures, and hypersensitivity to penicillins, cephalosporins, or other beta-lactam antibiotics. Avoid administering to children younger than 12 years with CNS infections.

Levofloxacin (Levaquin)

Levofloxacin is rapidly becoming a popular choice in pneumonia; this agent is a fluoroquinolone used to treat CAP caused by S aureus, S pneumoniae (including penicillin-resistant strains), H influenzae, H parainfluenzae, Klebsiella pneumoniae, M catarrhalis, C pneumoniae, Legionella pneumophila, or M pneumoniae. Fluoroquinolones should be used empirically in patients likely to develop exacerbation due to resistant organisms to other antibiotics.

Levofloxacin is the L stereoisomer of the D/L parent compound ofloxacin, the D form being inactive. It has good monotherapy with extended coverage against Pseudomonas species and excellent activity against pneumococcus. Levofloxacin acts by inhibition of DNA gyrase activity. The oral form has a bioavailability that is reportedly 99%.

The 750-mg dose is as well tolerated as the 500-mg dose, and it is more effective. Other fluoroquinolones with activity against S pneumoniae may be useful and include moxifloxacin, gatifloxacin, and gemifloxacin

Clarithromycin (Biaxin)

Clarithromycin is another initial drug of choice that is used in otherwise uncomplicated pneumonia. It is used to treat CAP caused by H influenzae, M pneumoniae, S pneumoniae, M catarrhalis, H parainfluenzae, or C pneumoniae (TWAR strain). Clarithromycin appears to cause more GI symptoms (eg, gastric upset, metallic taste) than azithromycin.

This agent is a semisynthetic macrolide antibiotic that reversibly binds to the P site of the 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.

Erythromycin (E.E.S., E-Mycin, Eryc, Ery-Tab, Erythrocin)

Erythromycin covers most potential etiologic agents, including Mycoplasma species. The oral regimen may be insufficient to adequately treat Legionella species, and this agent is less active against H influenzae. Although the standard course of treatment is 10 days, treatment until the patient has been afebrile for 3-5 days seems a more rational approach. Erythromycin therapy may result in GI upset, causing some clinicians to prescribe an alternative macrolide or change to a tid dosing.

Erythromycin is a macrolide that inhibits bacterial growth possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Vancomycin (Vancocin)

Vancomycin is classified as a glycopeptide agent that has excellent gram-positive coverage, including methicillin-resistant S aureus (MRSA). To avoid toxicity, current recommendations indicate to assay vancomycin trough levels after the third dose drawn 0.5 hour before the next dosing. Use CrCl to adjust the dose in patients diagnosed with renal impairment.

Telavancin (Vibativ)

Telavancin is a lipoglycopeptide antibacterial that is a synthetic derivative of vancomycin. It is indicated for treatment of adults with hospital-acquired and ventilator-associated bacterial pneumonia (HABP/VABP), caused by susceptible isolates of Staphylococcus aureus, including methicillin-susceptible and resistant isolates. This agent is reserved for use when alternative treatments are not suitable.

Meropenem (Merrem IV)

Meropenem is indicated for community-acquired pneumonia, including multi–drug-resistant S pneumoniae. This agent is a bactericidal broad-spectrum carbapenem antibiotic that inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription, and inhibits cell wall synthesis.

Meropenem is effective against most gram-positive and gram-negative bacteria and has slightly increased activity against gram-negatives and slightly decreased activity against staphylococci and streptococci compared with imipenem.

Ceftolozane/tazobactam (Zerbaxa)

Ceftolozane is a cephalosporin that has demonstrated potent in vitro activity against Pseudomonas aeruginosa. Tazobactam is a beta-lactamase inhibitor. It is indicated for treatment of hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia (HABP/VABP) caused by the following susceptible gram-negative microorganisms: Enterobacter cloacae, Escherichia coli, Haemophilus influenzae, Klebsiella oxytoca, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, and Serratia marcescens.

Moxifloxacin (Avelox)

Moxifloxacin is a fluoroquinolone that inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. Use caution in prolonged therapy, and perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic). Note that superinfections may occur with prolonged or repeated antibiotic therapy, and fluoroquinolones have induced seizures in patients with CNS disorders as well as caused tendinitis or tendon rupture.

Lefamulin (Xenleta)

Lefamulin is a first-in-class pleuromutilin antibacterial. It inhibits bacterial protein synthesis through interactions (hydrogen bonds, hydrophobic interactions, and Van der Waals forces) with the A- and P-sites of the peptidyl transferase center (PTC) in domain V of the 23s rRNA of the 50S subunit. It is indicated for adults with bacterial CAP caused by S pneumoniae, S aureus (methicillin-susceptible isolates), H influenzae, Legionella pneumophila, M pneumoniae, or C pneumoniae.

Ampicillin (Principen)

Ampicillin is a broad-spectrum penicillin that interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. This agent is used as an alternative drug to amoxicillin when the patient is unable to take oral medication.

Previously, HACEK bacteria (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) were uniformly susceptible to ampicillin; however, beta-lactamase–producing strains of HACEK have been identified.

Penicillin G (Pfizerpen)

Penicillin G interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Piperacillin and tazobactam sodium (Zosyn)

The piperacillin and tazobactam sodium combination is an antipseudomonal penicillin plus beta-lactamase inhibitor. This agent inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication.

Perform CBC counts before the initiation of therapy and at least weekly during therapy. In addition, monitor for liver function abnormalities by measuring AST and ALT levels during therapy, and perform urinalysis and BUN and creatinine determinations during therapy. Adjust the dose if laboratory values become elevated, and monitor blood levels to avoid possible neurotoxic reactions.

Ceftaroline (Teflaro)

Ceftaroline is a fifth-generation cephalosporin indicated for community-acquired bacterial pneumonia and for acute bacterial skin and skin structure infections, including methicillin-resistant Staphylococcus aureus (MRSA). This agent is a beta-lactam cephalosporin with activity against aerobic and anaerobic gram-positive and aerobic gram-negative bacteria. It demonstrates activity in vivo against resistant MRSA strains and activity in vitro against vancomycin-resistant and linezolid-resistant S aureus

Cefprozil (Cefzil)

Cefprozil binds to one or more of the penicillin-binding proteins, inhibiting cell wall synthesis and resulting in bactericidal activity. Use this agent with caution in patients with renal impairment (coadministration with furosemide and aminoglycosides increases nephrotoxic effects). Probenecid coadministration also increases the effect of cefprozil

Ticarcillin and clavulanate (Timentin)

It inhibits biosynthesis of the cell wall mucopeptide and is effective during the stage of active growth.

It is an antipseudomonal penicillin plus a beta-lactamase inhibitor that provides coverage against most gram-positive, most gram-negative, and most anaerobic bacteria

Omadacycline (Nuzyra)

Omadacycline is an aminomethylcycline antibacterial within the tetracycline drug class that binds to the 30S ribosomal subunit and blocks protein synthesis. It is active in vitro against gram-positive bacteria expressing tetracycline resistance active efflux pumps (tetK and tet L) and ribosomal protection proteins (tet M). It is indicated for the treatment of community-acquired bacterial pneumonia (CABP) in adults caused by susceptible microorganisms, including Streptococcus pneumoniae, Staphylococcus aureus (methicillin-susceptible isolates), Haemophilus influenzae, Haemophilus parainfluenzae, Klebsiella pneumoniae, Legionella pneumophila, Mycoplasma pneumoniae, and Chlamydophila pneumoniae. Omadacycline is available for intravenous or oral administration.

Glucocorticoids

Class Summary

Glucocorticoids have anti-inflammatory properties and cause profound and varied metabolic effects. Agents with corticosteroid activity modify the body's immune response to diverse stimuli.

Hydrocortisone (AHydrocort, Alphosyl, Aquacort)

Hydrocortisone is the drug of choice because of its mineralocorticoid activity and glucocorticoid effects.

Vaccines

Class Summary

Pneumococcal vaccines are recommended as part of routine prophylaxis in young children (aged < 5 y) and adults aged 65 y or older. These vaccines are also recommended for individuals who are immunocompromised (eg, HIV, cancer, renal disease), or have functional or anatomic asplenia, cerebrospinal fluid leaks, or cochlear implants.

Pneumococcal vaccine 13-valent (Prevnar 13)

Capsular polysaccharide vaccine against 13 strains of S pneumoiae, conjugated to nontoxic diphtheria protein, including serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and 23F.

Pneumococcal vaccine polyvalent (Pneumovax 23)

S pneumonia capsular antigens stimulate active immune response resulting in production of endogenously produced antibodies. The 23 serotypes contained in the vaccine include: 1, 2, 3, 4, 5, 6B, 7F, 8, 9N, 9V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19F, 19A, 20, 22F, 23F, and 33F.

 

Questions & Answers

Overview

What is bacterial pneumonia?

What are the symptoms of bacterial pneumonia, and which pathogens may be involved?

What are the signs of bacterial pneumonia?

What are physical findings in bacterial pneumonia?

Which exam findings may indicate a specific etiology for bacterial pneumonia?

Which assessments are used to evaluate the severity of bacterial pneumonia?

When should a sputum Gram stain be performed in the workup of bacterial pneumonia?

Which imaging studies are used in the diagnosis of bacterial pneumonia?

What is the role of bronchoscopy in the diagnosis of bacterial pneumonia?

When is a thoracentesis used in the diagnosis of bacterial pneumonia?

Which pathogen-specific tests are used in the diagnosis of bacterial pneumonia?

What information does histology provide in the diagnosis of bacterial pneumonia?

What is the role of antibiotics in the treatment of bacterial pneumonia?

What supportive measures are used in the treatment of bacterial pneumonia?

How is bacterial pneumonia defined?

What is community-acquired pneumonia (CAP)?

What is aspiration pneumonia?

What causes bacterial pneumonia?

What are the distinguishing characteristics of bacterial pneumonia?

How is the anatomic or radiologic distribution of bacterial pneumonia characterized?

Which environmental settings are associated with bacterial pneumonia?

What is institutional-acquired pneumonia (IAP), and what are the risk factors for healthcare-associated pneumonia (HCAP)?

What is nursing home-acquired pneumonia (NHAP)?

What are the atypical signs commonly seen in nursing home patients with bacterial pneumonia?

What are the IDSA and ATS guidelines on the classification of bacterial pneumonia?

What is nosocomial pneumonia?

What is hospital-acquired pneumonia (HAP), and what are the risk factors?

What is ventilator-associated pneumonia (VAP), and how common is it?

What are the risk factors for aspiration pneumonia?

What causes an increased risk of aspiration and bacterial pneumonia in critically ill patients?

Which bacteria are associated with aspiration pneumonia?

What causes the development of bacterial pneumonia?

What is the pathophysiology of bacterial pneumonia?

What is the effect of acute inflammation during pulmonary infection?

What are the mechanisms that increase virulence in bacterial pneumonia?

What are the organism-specific virulence factors of Streptococcus pneumoniae and Pseudomonas aeruginosa in bacterial pneumonia?

What deficiencies in host defenses can predispose a patient to bacterial pneumonia?

What is the role of viral infection in bacterial pneumonia?

What are the effects of interactions between viruses and bacteria in bacterial pneumonia?

Which pathogens mostly commonly cause bacterial pneumonia?

What are the risk factors for bacterial pneumonia?

Which gram-positive bacteria can cause bacterial pneumonia?

Which gram-negative bacteria can cause bacterial pneumonia?

Which atypical organisms can cause bacterial pneumonia?

Which anaerobic organisms can cause bacterial pneumonia?

What are the most common etiologies of community-acquired pneumonia (CAP) in the hospital setting?

How common are acute lower respiratory tract infections?

What is the incidence of pneumonia in the US?

What are the most common etiologies of community-acquired pneumonia (CAP) in the outpatient setting?

What are the most common etiologies of community-acquired pneumonia (CAP) in ICU?

How common is ventilator-associated pneumonia (VAP) and what is the mortality rate?

What are the race-related demographics of bacterial pneumonia?

What are the sex-related demographics of bacterial pneumonia?

What are the age-related demographics and mortality rates of bacterial pneumonia?

What is the prognosis of bacterial pneumonia, and which factors contribute to increased morbidity and mortality?

What is the risk of mortality in bacterial pneumonia?

What is the microbial etiology of mortality in bacterial pneumonia?

What morbidities are associated with bacterial pneumonia?

Which preventive measures should be encouraged in patients with bacterial pneumonia?

What patient education information is available on bacterial pneumonia?

Presentation

Which features of the patient’s history should be included in the intake assessment of bacterial pneumonia?

What potential exposures are significant in determining possible etiologies of bacterial pneumonia?

What are the aspiration risk factors that increase the risk of developing secondary bacterial pneumonia?

Which factors other than exposures are important in the evaluation of bacterial pneumonia?

What is the clinical presentation of bacterial pneumonia?

What do the characteristics of the sputum suggest in bacterial pneumonia?

What nonspecific symptoms are common in bacterial pneumonia?

How is pertussis characterized in patients with bacterial pneumonia?

When does pneumonia from H influenzae most commonly occur and who is most affected?

What is the presentation of Legionella pneumonia?

What is Legionella pneumophila?

How can physical exam findings vary in patients with bacterial pneumonia?

What are the signs of bacterial pneumonia?

What are the physical findings in bacterial pneumonia?

Which exam findings are associated with a specific etiology for bacterial pneumonia?

What is the CURB-65 scoring system for the risk stratification of bacterial pneumonia?

Which assessments can be used to determine if outpatient treatment or hospitalization is indicated in community-acquired pneumonia (CAP)?

What are the guidelines for determining the treatment setting for bacterial pneumonia based on the CURB-65 score?

What are the mortality rates for each of the CURB-65 scores in bacterial pneumonia?

What is the pneumonia severity index (PSI) for the risk stratification of bacterial pneumonia?

How are demographic factors scored in the pneumonia severity index (PSI) for bacterial pneumonia?

How are coexisting illnesses scored in the pneumonia severity index (PSI) for bacterial pneumonia?

How are physical exam findings scored in the pneumonia severity index (PSI) for bacterial pneumonia?

How are lab and radiographic findings scored in the pneumonia severity index (PSI) for bacterial pneumonia?

What are the mortality rates for each class of the pneumonia severity index (PSI)?

What are the guidelines on treatment setting based on the pneumonia severity index (PSI) risk class in bacterial pneumonia?

What considerations are important when using indices and scores for risk stratification of bacterial pneumonia?

How accurate are the CURB-65 and pneumonia severity index (PSI) in risk stratification for bacterial pneumonia?

What are the IDSA/ATS criteria for determining the appropriate care setting in community-acquired pneumonia (CAP)?

When is direct admission to an ICU mandated for patients with bacterial pneumonia?

Which biological markers may be used for the diagnosis and prognostication of bacterial pneumonia?

In addition to CURB-65 and pneumonia severity index (PSI), what other scoring models can be used to predict mortality in severe bacterial pneumonia?

How is the SOAR scoring model used to predict 30-day mortality in patients with nursing home-acquired pneumonia (NHAP)?

What other prediction models regarding pneumonia severity and outcomes are currently in development?

What are the potential complications of bacterial pneumonia?

How do parapneumonic effusions and empyema occur in bacterial pneumonia?

DDX

What is the most prevalent causative organism in bacterial pneumonia?

How is a diagnosis of aspiration made in bacterial pneumonia?

When should Legionella pneumonia be considered in the diagnosis of bacterial pneumonia?

Which aspects of disease are important in the evaluation and management of bacterial pneumonia?

How is bacterial pneumonia distinguished from other pulmonary diseases?

Why is the differentiation between community-acquired pneumonia (CAP), healthcare-associated pneumonia (HCAP), hospital-acquired pneumonia (HAP), and other pulmonary pathology important?

Which conditions should be considered in children with symptoms of bacterial pneumonia?

What are the differential diagnoses for Bacterial Pneumonia?

Workup

What is the role of diagnostic testing in suspected bacterial pneumonia?

Which lab values may be associated with Legionella pneumonia?

What is the role of antigen-antibody testing in the workup of Legionella pneumonia?

What is the role of imaging studies in the workup of bacterial pneumonia?

Which lab tests are useful for classifying illness severity and admission decisions in bacterial pneumonia?

What do pulse oximetry findings and C-reactive protein (CRP) levels contribute to the clinical picture of bacterial pneumonia?

What may be indicated by leukocytosis or leukopenia in bacterial pneumonia?

What is the significance of an elevated INR in the workup of bacterial pneumonia?

What is the role of blood cultures in bacterial pneumonia?

What is the role of sputum evaluation in the workup of bacterial pneumonia?

Which sputum specimens are suitable for culture in bacterial pneumonia?

How are sputum samples for stains and cultures obtained in intubated patients with bacterial pneumonia?

What is the role of chest radiography in the workup of bacterial pneumonia?

How are the radiographic findings of lobar pneumonia characterized in bacterial pneumonia?

What are the radiographic findings of S pneumoniae lobar pneumonia?

What are the radiographic findings of aspiration lobar pneumonia?

What are the radiographic findings of K pneumoniae lobar pneumonia?

What are the radiographic findings of Legionella lobar pneumonia?

What is the radiographic appearance of lobar pneumonia?

What are the radiographic findings of bronchopneumonia?

What are the radiographic findings of S aureus pneumonia?

What are the radiographic findings of P aeruginosa pneumonia?

What are radiographic findings of interstitial pneumonia?

What is the role of CT scanning in the diagnosis of bacterial pneumonia?

Which abnormalities cause increased lung opacity on CT scans in bacterial pneumonia?

Which abnormalities cause decreased lung opacity on CT scans in bacterial pneumonia?

What is the role of chest ultrasonography in the workup of bacterial pneumonia?

What is the role of thoracentesis in the workup of bacterial pneumonia?

What pathogen-specific tests are available for the workup of bacterial pneumonia?

How are histologic inflammatory lung changes described in bacterial pneumonia?

How are the stages of inflammatory response in lobar pneumonia characterized?

What are the histologic characteristics of bronchopneumonia?

What are the histologic characteristics of interstitial pneumonia?

How are bronchoscopy and bronchoalveolar lavage (BAL) used in the workup of bacterial pneumonia?

Treatment

What is the first step in the management of bacterial pneumonia?

Which index can be used to guide inpatient care and mortality risk for bacterial pneumonia, and how accurate is it?

When is direct admission to an ICU mandated for the treatment of bacterial pneumonia?

Which patients with bacterial pneumonia must be stabilized before transfer?

What are the treatments for bacterial pneumonia and bronchospasm?

What treatment is used for mild shortness of breath in bacterial pneumonia?

What treatments are available for moderate dyspnea in bacterial pneumonia?

What alternatives to intubation can be used for refractory hypoxemia in bacterial pneumonia?

What is the role of fluid resuscitation in the treatment of bacterial pneumonia?

How is empiric antibiotic therapy used in the treatment of bacterial pneumonia?

What are the guidelines for evaluation and antibiotic treatment of community-acquired pneumonia (CAP)?

What are the guidelines for the treatment of hypotension due to septic shock in bacterial pneumonia?

How effective are corticosteroids in the treatment of bacterial pneumonia?

Is drotrecogin alfa used in the treatment of bacterial pneumonia?

What are the goals of pharmacotherapy for bacterial pneumonia?

What is the role of antimicrobial therapy in the treatment of bacterial pneumonia?

What are the IDSA/ATS treatment guidelines for community-acquired pneumonia (CAP)?

How is an antibiotic agent selected for hospitalized patients in the treatment of bacterial pneumonia?

Which infection should always be considered when evaluating community-acquired pneumonia (CAP)?

How is initial antibiotic therapy selected for hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)?

How is empiric antibiotic therapy selected for outpatient treatment of bacterial pneumonia?

Which empiric antibiotic therapy is indicated in previously healthy patients with bacterial pneumonia and no exposure to antibiotics within the previous 90 days?

Which empiric antibiotic therapy is indicated in patients with bacterial pneumonia and comorbidities or use of antimicrobials within the last 90 days?

Which empiric antibiotic therapy is indicated in patients with bacterial pneumonia and exposure to antibiotics within the previous 90 days?

What are the CMS and Joint Commission guidelines for initiating empiric antibiotic therapy in inpatients with bacterial pneumonia?

Which empiric antibiotics are indicated in non- ICU or ward patients with bacterial pneumonia?

Which empiric antibiotics are indicated in ICU patients with bacterial pneumonia?

Which empiric antibiotics are indicated in bacterial pneumonia with an increased risk of Pseudomonas infection?

Which empiric antibiotics are indicated in patients with bacterial pneumonia and a greater risk of anaerobic infection?

Which empiric antibiotics are indicated in patients with bacterial pneumonia and suspected MRSA infection?

Why is the prevention of influenza important?

Which supportive measures are indicated in the management of bacterial pneumonia?

When is clinical response to antibiotic therapy evaluated and adjusted in bacterial pneumonia?

When is resolution of pneumococcal pneumonia demonstrated on chest radiography?

What does a lack of response to treatment for bacterial pneumonia suggest?

Which studies are indicated in unresponsive cases of bacterial pneumonia?

What are the guidelines on pneumococcal vaccinations for the prevention of bacterial pneumonia?

How effective are influenza vaccinations in reducing the rate of hospitalization for pneumonia and influenza in elderly persons?

How effective are pneumococcal vaccines in the prevention of bacterial pneumonia, and who is at highest risk for pneumococcal pneumonia?

Which vaccines are effective in the prevention of invasive pneumococcal disease?

What are the recommendations for pneumococcal vaccinations for the prevention of bacterial pneumonia?

What is the role of smoking cessation in the prevention of pneumonia and influenza?

Which strategies are effective in the prevention of nosocomial pneumonia?

Which consultations are recommended in bacterial pneumonia?

What is the recommended follow-up for patients with bacterial pneumonia who are treated as outpatients?

When should patients with bacterial pneumonia have follow-up chest radiography, and which findings indicate the need for further treatment?

How common is lung cancer following bacterial pneumonia?

Medications

What is the mainstay of drug therapy for bacterial pneumonia?

What is the role of glucocorticoids in the treatment of acute bacterial pneumonia?

What is the standard treatment for outpatients with bacterial pneumonia?

What is the standard treatment for bacterial pneumonia in children younger than 5 years?

What is the standard outpatient treatment for mild-to-moderate pneumonias in children?

Who is at risk for H influenzae type B (HIB) infection, and what is the standard outpatient treatment?

What is the role of macrolides in the treatment of bacterial pneumonia?

What are the adverse effects of macrolides in the treatment of bacterial pneumonia?

When are macrolides indicated for the treatment of bacterial pneumonia?

When are parenteral agents indicated in the treatment of bacterial pneumonia?

What are the benefits of using second-generation cephalosporins for the treatment of bacterial pneumonia?

What are the benefits of using third-generation cephalosporins for the treatment of bacterial pneumonia?

How is TMP-SMZ used in the treatment of bacterial pneumonia, and what are the adverse effects?

What is the recommended treatment for a severely ill patient with features of sepsis, respiratory failure, or neutropenia in the setting of bacterial pneumonia?

Which medications in the drug class Antibiotics are used in the treatment of Bacterial Pneumonia?

Which medications in the drug class Glucocorticoids are used in the treatment of Bacterial Pneumonia?

Which medications in the drug class Vaccines are used in the treatment of Bacterial Pneumonia?