Updated: Dec 07, 2016 Author: Justina Gamache, MD Chief Editor: Guy W Soo Hoo, MD, MPH

Bacterial Pneumonia
Updated: Dec 07, 2016

Author: Justina Gamache, MD; Chief Editor: Guy W Soo Hoo, MD, MPH
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.
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).
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Signs and symptoms
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
 Bullous myringitis: May indicate Mycoplasma pneumoniae infection
 Cutaneous nodules: May suggest Nocardia infection
 Decreased gag reflex: Suggests risk for aspiration
See Clinical Presentation for more detail.
Diagnosis
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
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 pneumonia. Chest radiograph shows dense consolidation in both lower lobes.
View Media Gallery
A 40-year-old patient with

Chlamydia pneumonia. Chest radiograph shows multifocal, patchy consolidation in the
right upper, middle, and lower lobes.
View Media Gallery
A 38-year-old patient with
Mycoplasma pneumonia. Chest radiograph shows a vague, ill-defined opacity in the left
lower lobe.
View Media Gallery
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]
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 patient with right upper lobe pneumonia. Note the increased
anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary
disease (COPD).
View Media Gallery
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
View Media Gallery
Bacterial pneumonia. Radiographic images in a patient
with early right middle lobe pneumonia.
View Media Gallery
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. [9] 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. [10] Based on this meta-analysis, the 2016 IDSA and ATS guidelines have called for
the removal of the concept of HCAP, [9] 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. [11]
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. [12] 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. [13]
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. [14] 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. [15]
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.[16]
 Pseudomonas aeruginosa - Pili play important role in the attachment to host cells. A
type III secretion system allows injection of toxins into host cells. [17]
Host resistance
Deficits in various host defenses and an inability to mount an appropriate acute
inflammatory response can predispose patients to infection, as follows [15] :
 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. [18] 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. [19] 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. [18]
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. [18]
Etiology
Although pneumonia may be caused by myriad pathogens, a limited number of agents are
responsible for most cases, [3, 20, 21, 22] 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. [23] However, pregnant patients with H1N1
influenza in the 2009 pandemic were at increased risk of developing
secondary Klebsiella pneumonia with poor clinical outcome. [24]
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-resistantEnterococcus (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. [25]
 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. [20, 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.Legionella pneumophila 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, andPrevotella.
Epidemiology
In the United States, acute lower respiratory tract infections cause more disease and death
than any other infection. [15] In fact, these infections also cause a greater burden of disease
worldwide than human immunodeficiency virus (HIV) infection, malaria, cancer, or heart
attacks. [15] 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, 26]
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. [27, 28]
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. [27, 28]
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. [27, 28]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%. [29]
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. [30]
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 Pneumonia Center, as well as Bacterial
Pneumonia and Viral Pneumonia.
Bacterial Pneumonia Treatment & Management

 Author: Justina Gamache, MD; Chief Editor: Guy W Soo Hoo, MD, MPH more...
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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. [37]
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 minimum 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. [60]
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. [61] 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
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. [62, 63]
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)
First-Line Alternative
Organism
Antimicrobials Antimicrobials
Streptococcus
pneumoniae
Penicillin Penicillin G, amoxicillin Macrolide,

susceptible cephalosporin
(oral or
parenteral),
clindamycin,
(MIC < 2 doxycycline,
mcg/mL) respiratory
fluoroquinolone
Penicillin
resistant
Vancomycin,
linezolid, high-
Agents chosen on the
dose amoxicillin
(MIC ≥2 basis of sensitivity
(3 g/d with MIC
mcg/mL)
≤4 mcg/mL
Staphylococcus aureus
Methicillin Antistaphylococcal Cefazolin,

susceptible penicillin clindamycin
Methicillin Trimethoprim-
Vancomycin, linezolid
resistant sulfamethoxazole
Haemophilus
influenzae
Fluoroquinolone,
Non–beta-
doxycycline,
lactamase Amoxicillin
azithromycin,
producing
clarithromycin
Second- or third- Fluoroquinolone,

Beta-lactamase generation doxycycline,
producing cephalosporin, azithromycin,
amoxicillin/clavulanate clarithromycin
Mycoplasma Macrolide,
Fluoroquinolone
pneumoniae tetracycline
Chlamydophila Macrolide,
Fluoroquinolone
pneumoniae tetracycline
Fluoroquinolone,
Legionella species Doxycycline
azithromycin
Chlamydophila psittaci Tetracycline Macrolide
Coxiella burnetii Tetracycline Macrolide
Gentamicin,
Francisella tularensis Doxycycline
streptomycin
Streptomycin, Doxycycline,
Yersinia pestis
gentamicin fluoroquinolone
Other
Ciprofloxacin, fluoroquinolones, beta-
Bacillus
levofloxacin, lactam (if susceptible),
anthracis(inhalational)
doxycycline rifampin, clindamycin,
chloramphenicol
Third-generation Beta-lactam/beta-
Enterobacteriaceae cephalosporin, lactamase inhibitor,
carbapenem fluoroquinolone
Antipseudomonal
beta-lactam plus Aminoglycoside plus
Pseudomonas
ciprofloxacin, ciprofloxacin or
aeruginosa
levofloxacin, or levofloxacin
aminoglycoside
Trimethoprim-
Bordetella pertussis Macrolide
sulfamethoxazole
Anaerobe (aspiration) Beta- Carbapenem

lactam/beta-
lactamase
inhibitor,
clindamycin
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, [64] 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, 14] :
 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.[65] 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. [66]
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. [19]
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. [67] Evaluation of 77 postmortem lung specimens by the CDC
revealed that 29% of those that died also had evidence of bacterial coinfection. [68]
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. [19]
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 recommendatoins
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 [69, 70] :
 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. [71]
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. [72] 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. [73]
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. [74]
Bacterial Pneumonia Medication

 Author: Justina Gamache, MD; Chief Editor: Guy W Soo Hoo, MD, MPH more...
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Medication SummaryGlucocorticoidsOutpatient/inpatient antibiotic
administrationPediatric antimicrobial therapyMacrolidesCephalosporinsCombination
drugs
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.
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, [61] 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.
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.
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 andMycoplasma 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.
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).
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.
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. [75]
Antibiotics
Class Summary
Empiric antimicrobial therapy must be comprehensive and should cover all likely
pathogens in the context of the clinical setting.
Azithromycin (Zithromax)
 View full drug information
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. Due
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.
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.
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.
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
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 (Cortef, Hydrocort, Hydrocortone)
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.
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