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Overview of community-acquired pneumonia in adults

Author: Julio A Ramirez, MD, FACP
Section Editor: Thomas M File, Jr, MD
Deputy Editor: Sheila Bond, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2022. | This topic last updated: Apr 15, 2022.
INTRODUCTION
Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality

worldwide. The clinical presentation of CAP varies, ranging from mild pneumonia
characterized by fever and productive cough to severe pneumonia characterized by
respiratory distress and sepsis. Because of the wide spectrum of associated clinical features,
CAP is a part of the differential diagnosis of nearly all respiratory illnesses.
This topic provides a broad overview of the epidemiology, microbiology, pathogenesis, clinical
features, diagnosis, and management of CAP in immunocompetent adults. Detailed
discussions of each of these issues are presented separately; links to these discussions are
provided within the text below.
DEFINITIONS
Pneumonia is frequently categorized based on site of acquisition ( table 1).
● Community-acquired pneumonia (CAP) refers to an acute infection of the pulmonary

parenchyma acquired outside of the hospital.
● Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma

acquired in hospital settings and encompasses both hospital-acquired pneumonia
(HAP) and ventilator-associated pneumonia (VAP).
• HAP refers to pneumonia acquired ≥48 hours after hospital admission.

infoestrategica.uaeh.elogim.com/index.php/uptodate 1/74
• VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.
Health care-associated pneumonia (HCAP; no longer used) referred to pneumonia acquired in

health care facilities (eg, nursing homes, hemodialysis centers) or after recent hospitalization.
The term HCAP was used to identify patients at risk for infection with multidrug-resistant
pathogens. However, this categorization may have been overly sensitive, leading to increased,
inappropriately broad antibiotic use and was thus retired. In general, patients previously
classified as having HCAP should be treated similarly to those with CAP. (See "Epidemiology,
pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated
pneumonia in adults".)
EPIDEMIOLOGY
Incidence — CAP is one of the most common and morbid conditions encountered in clinical
practice [1-3]. In the United States, CAP accounts for over 4.5 million outpatient and emergency
room visits annually, corresponding to approximately 0.4 percent of all encounters [4]. CAP is
the second most common cause of hospitalization and the most common infectious cause of
death [5,6]. Approximately 650 adults are hospitalized with CAP every year per 100,000
population in the United States, corresponding to 1.5 million unique CAP hospitalizations each
year [7]. Nearly 9 percent of patients hospitalized with CAP will be rehospitalized due to a new
episode of CAP during the same year.
Risk factors
● Older age – The risk of CAP rises with age [7,8]. The annual incidence of hospitalization
for CAP among adults ≥65 years old is approximately 2000 per 100,000 in the United
States [7,9]. This figure is approximately three times higher than the general population
and indicates that 2 percent of the older adult population will be hospitalized for CAP
annually ( figure 1).
● Chronic comorbidities – The comorbidity that places patients at highest risk for CAP
hospitalization is chronic obstructive pulmonary disease (COPD), with an annual
incidence of 5832 per 100,000 in the United States [7]. Other comorbidities associated
with an increased incidence of CAP include other forms of chronic lung disease (eg,
bronchiectasis, asthma), chronic heart disease (particularly congestive heart failure),
stroke, diabetes mellitus, malnutrition, and immunocompromising conditions
( figure 2) [7,10,11].
● Viral respiratory tract infection – Viral respiratory tract infections can lead to primary
viral pneumonias and also predispose to secondary bacterial pneumonia. This is most
pronounced for influenza virus infection. (See "Seasonal influenza in adults: Clinical
manifestations and diagnosis", section on 'Pneumonia'.)
● Impaired airway protection – Conditions that increase risk of macroaspiration of

stomach contents and/or microaspiration of upper airway secretions predispose to CAP,
such as alteration in consciousness (eg, due to stroke, seizure, anesthesia, drug or
alcohol use) or dysphagia due to esophageal lesions or dysmotility.
● Smoking and alcohol overuse – Smoking, alcohol overuse (eg, >80 g/day), and opioid
use are key modifiable behavioral risk factors for CAP [7,10,12,13].
● Other lifestyle factors – Other factors that have been associated with an increased risk
of CAP include crowded living conditions (eg, prisons, homeless shelters), residence in
low-income settings, and exposure to environmental toxins (eg, solvents, paints, or
gasoline) [7,10,11,14].
Combinations of risk factors, such as smoking, COPD, and congestive heart failure, are
additive in terms of risk [15]. These risk factors and other predisposing conditions for the
development of CAP are discussed separately. (See "Epidemiology, pathogenesis, and
microbiology of community-acquired pneumonia in adults", section on 'Predisposing host
conditions'.)
MICROBIOLOGY
Common causes — Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the

most frequently detected pathogens in patients with CAP [8,16]. However, in a large proportion
of cases (up to 62 percent in some studies performed in hospital settings), no pathogen is
detected despite extensive microbiologic evaluation [8,17,18].
The most commonly identified causes of CAP can be grouped into three categories:
● Typical bacteria
• S. pneumoniae (most common bacterial cause)

• Haemophilus influenzae
• Moraxella catarrhalis
• Staphylococcus aureus
Group A streptococci
• Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or

Escherichia coli)
• Microaerophilic bacteria and anaerobes (associated with aspiration)
● Atypical bacteria ("atypical" refers to the intrinsic resistance of these organisms to beta-
lactams and their inability to be visualized on Gram stain or cultured using traditional
techniques)
• Legionella spp
• Mycoplasma pneumoniae
• Chlamydia pneumoniae
• Chlamydia psittaci
• Coxiella burnetii
● Respiratory viruses
• Influenza A and B viruses

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
• Other coronaviruses (eg, CoV-229E, CoV-NL63, CoV-OC43, CoV-HKU1)
• Rhinoviruses
• Parainfluenza viruses
• Adenoviruses
• Respiratory syncytial virus
• Human metapneumovirus
• Human bocaviruses
The relative prevalence of these pathogens varies with geography, pneumococcal vaccination
rates, host risk factors (eg, smoking), season, and pneumonia severity ( table 2).
Certain epidemiologic exposures also raise the likelihood of infection with a particular
pathogen ( table 3). As examples, exposure to contaminated water is a risk factor for
Legionella infection, exposure to birds raises the possibility of C. psittaci infection, travel or
residence in the southwestern United States should raise suspicion for coccidioidomycosis,
and poor dental hygiene may predispose patients with pneumonia caused by oral flora or
anaerobes. In immunocompromised patients, the spectrum of possible pathogens also
broadens to include fungi and parasites as well as less common bacterial and viral pathogens.
(See "Epidemiology of pulmonary infections in immunocompromised patients" and "Approach
to the immunocompromised patient with fever and pulmonary infiltrates".)
While the list above details some of most common causes of CAP, >100 bacterial, viral, fungal,
and parasitic causes have been reported. (See "Epidemiology, pathogenesis, and microbiology
of community-acquired pneumonia in adults", section on 'Microbiology'.)
Important trends — Both the distribution of pathogens that cause CAP and our knowledge of
these pathogens are evolving. Key observations that have changed our understanding of CAP
and influenced our approach to management include:
● Decline in S. pneumoniae incidence – Although S. pneumoniae (pneumococcus) is the

most commonly detected bacterial cause of CAP in most studies, the overall incidence of
pneumococcal pneumonia is decreasing. This is in part due to widespread use of
pneumococcal vaccination, which results in both a decline in the individual rates of
pneumococcal pneumonia and herd immunity in the population. (See "Pneumococcal
pneumonia in patients requiring hospitalization", section on 'Prevalence'.)
Because pneumococcal vaccination rates vary regionally, the prevalence of S. pneumoniae

infection also varies. As an example, S. pneumoniae is estimated to cause approximately 30
percent of cases of CAP in Europe but only 10 to 15 percent in the United States, where
the population pneumococcal vaccination rate is higher [8].
● The coronavirus disease 2019 (COVID-19) pandemic – SARS-CoV-2 is an important cause

of CAP and is discussed in detail elsewhere. (See "COVID-19: Epidemiology, virology, and
prevention".)
● Increased recognition of other respiratory viruses – Respiratory viruses have been

detected in approximately one-third of cases of CAP in adults when using molecular
methods [8]. The extent to which respiratory viruses serve as single pathogens, cofactors
in the development of bacterial CAP, or triggers for dysregulated host immune response
has not been established.
● Low overall rate of pathogen detection – Despite extensive evaluation using molecular
diagnostics and other microbiologic testing methods, a causal pathogen can be identified
in only half of cases of CAP. This finding highlights that our understanding of CAP
pathogenesis is incomplete. As molecular diagnostics become more advanced and use
broadens, our knowledge is expected to grow.
● Discovery of the lung microbiome – Historically, the lung has been considered sterile.
However, culture-independent techniques (ie, high throughput 16S ribosomal ribonucleic
acid [rRNA] gene sequencing) have identified complex and diverse communities of
microbes that reside within the alveoli [19-21]. This finding suggests that resident alveolar
microbes play a role in the development of pneumonia, either by modulating the host
immune response to infecting pathogens or through direct overgrowth of specific
pathogens within the alveolar microbiome. (See 'Pathogenesis' below.)
Antimicrobial resistance — Knowledge of antimicrobial resistance patterns and risk factors

for infection with antimicrobial-resistant pathogens help inform the selection of antibiotics for
empiric CAP treatment ( table 4).
● S. pneumoniae may be resistant to one or more antibiotics commonly used for the
empiric treatment of CAP.
• Macrolide resistance rates vary regionally but are generally high (>25 percent) in the
United States, Asia, and southern Europe. Resistance rates tend to be lower in
northern Europe. (See "Resistance of Streptococcus pneumoniae to the macrolides,
azalides, lincosamides, and ketolides".)
• Estimates of doxycycline resistance are less certain and vary substantially worldwide.
In the United States, rates tend to be less than 20 percent but may be rising. (See
"Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and
trimethoprim-sulfamethoxazole".)
• Beta-lactam resistance rates also vary regionally but to a lesser extent than macrolide
and doxycycline resistance. In the United States, <20 percent of isolates are resistant
to penicillin and <1 percent to cephalosporins. (See "Resistance of Streptococcus
pneumoniae to beta-lactam antibiotics".)
• Fluoroquinolone resistance tends to be <2 percent in the United States but varies
regionally and with specific risk factors such as recent antibiotic use or
hospitalization. (See "Resistance of Streptococcus pneumoniae to the
fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole".)
Because resistance rates vary even at local levels, clinicians should refer to local
antibiograms to guide antibiotic selection when available. General epidemiologic data can
be obtained through sources such as the Center for Disease Dynamics, Economics &
Policy.
● Methicillin-resistant S. aureus (MRSA) is an uncommon cause of CAP. Risk factors for

MRSA have two patterns: health care associated and community acquired. The strongest
risk factors for MRSA pneumonia include known MRSA colonization or prior MRSA
infection, particularly involving the respiratory tract. Gram-positive cocci on sputum
Gram stain are also predictive of MRSA infection. Other factors that should raise
suspicion for MRSA infection include recent antibiotic use (particularly receipt of
intravenous antibiotics within the past three months), recent influenza-like illness, the
presence of empyema, necrotizing/cavitary pneumonia, and immunosuppression
( table 4).
In contrast with health care-associated MRSA, community-acquired MRSA (CA-MRSA)

infections tend to occur in younger healthy persons [22]. Risk factors for CA-MRSA
infection include a history of MRSA skin lesions, participation in contact sports, injection
drug use, crowded living conditions, and men who have sex with men. (See "Methicillin-
resistant Staphylococcus aureus (MRSA) in adults: Epidemiology".)
CAP caused by CA-MRSA can be severe and is associated with necrotizing and/or cavitary
pneumonia, empyema, gross hemoptysis, septic shock, and respiratory failure. These
features may be attributable to infection with toxin-producing CA-MRSA strains. In the
United States, these strains tend to be methicillin resistant and belong to the USA300
clone. (See "Virulence determinants of community-acquired methicillin-resistant
Staphylococcus aureus".)
● Pseudomonas is also an uncommon cause of CAP and tends to occur more frequently in
patients with known colonization or prior infection with Pseudomonas spp, recent
hospitalization or antibiotic use, underlying structural lung disease (eg, cystic fibrosis or
advanced chronic obstructive pulmonary disease [bronchiectasis]), and
immunosuppression. Antibiotic resistance is common among pseudomonal strains, and
empiric therapy with more than one agent that targets Pseudomonas is warranted for at-
risk patients with moderate to severe CAP ( table 4). (See "Pseudomonas aeruginosa
pneumonia" and 'Inpatient antibiotic therapy' below.)
PATHOGENESIS
Traditionally, CAP has been viewed as an infection of the lung parenchyma, primarily caused by
bacterial or viral respiratory pathogens. In this model, respiratory pathogens are transmitted
from person to person via droplets or, less commonly, via aerosol inhalation (eg, as with
Legionella or Coxiella species). Following inhalation, the pathogen colonizes the nasopharynx
and then reaches the lung alveoli via microaspiration. When the inoculum size is sufficient
and/or host immune defenses are impaired, infection results. Replication of the pathogen, the
production of virulence factors, and the host immune response lead to inflammation and
damage of the lung parenchyma, resulting in pneumonia ( figure 3).
With the identification of the lung microbiome, that model has changed [19-21]. While the
pathogenesis of pneumonia may still involve the introduction of respiratory pathogens into
the alveoli, the infecting pathogen likely has to compete with resident microbes to replicate. In
addition, resident microbes may also influence or modulate the host immune response to the
infecting pathogen. If this is correct, an altered alveolar microbiome (alveolar dysbiosis) may
be a predisposing factor for the development of pneumonia.
In some cases, CAP might also arise from uncontrolled replication of microbes that normally
reside in the alveoli. The alveolar microbiome is similar to oral flora and is primarily comprised
of anaerobic bacteria (eg, Prevotella and Veillonella) and microaerophilic streptococci [19-21].
Hypothetically, exogenous insults such as a viral infection or smoke exposure might alter the
composition of the alveolar microbiome and trigger overgrowth of certain microbes. Because
organisms that compose the alveolar microbiome typically cannot be cultivated using
standard cultures, this hypothesis might explain the low rate of pathogen detection among
patients with CAP.
In any scenario, the host immune response to microbial replication within the alveoli plays an
important role in determining disease severity. For some patients, a local inflammatory
response within the lung predominates and may be sufficient for controlling infection. In
others, a systemic response is necessary to control infection and to prevent spread or
complications, such as bacteremia. In a minority, the systemic response can become
dysregulated, leading to tissue injury, sepsis, acute respiratory distress syndrome, and/or
multiorgan dysfunction.
The pathogenesis of CAP is discussed in greater detail separately. (See "Epidemiology,

pathogenesis, and microbiology of community-acquired pneumonia in adults".)
CLINICAL PRESENTATION
The clinical presentation of CAP varies widely, ranging from mild pneumonia characterized by
fever, cough, and shortness of breath to severe pneumonia characterized by sepsis and
respiratory distress. Symptom severity is directly related to the intensity of the local and
systemic immune response in each patient.
● Pulmonary signs and symptoms – Cough (with or without sputum production),

dyspnea, and pleuritic chest pain are among the most common symptoms associated
with CAP. Signs of pneumonia on physical examination include tachypnea, increased work
of breathing, and adventitious breath sounds, including rales/crackles and rhonchi.
Tactile fremitus, egophony, and dullness to percussion also suggest pneumonia. These
signs and symptoms result from the accumulation of white blood cells (WBCs), fluid, and
proteins in the alveolar space. Hypoxemia can result from the subsequent impairment of
alveolar gas exchange. On chest radiograph, accumulation of WBCs and fluid within the
alveoli appears as pulmonary opacities ( image 1A-B).
● Systemic signs and symptoms – The great majority of patients with CAP present with
fever. Other systemic symptoms such as chills, fatigue, malaise, chest pain (which may be
pleuritic), and anorexia are also common. Tachycardia, leukocytosis with a leftward shift,
or leukopenia are also findings that are mediated by the systemic inflammatory
response. Inflammatory markers, such as the erythrocyte sedimentation rate (ESR), C-
reactive protein (CRP), and procalcitonin may rise, though the latter is largely specific to
bacterial infections. CAP is also the leading cause of sepsis; thus, the initial presentation
may be characterized by hypotension, altered mental status, and other signs of organ
dysfunction such as renal dysfunction, liver dysfunction, and/or thrombocytopenia [23].
Although certain signs and symptom such as fever, cough, tachycardia, and rales are common
among patients with CAP, these features are ultimately nonspecific and are shared among
many respiratory disorders (see 'Differential diagnosis' below). No individual symptom or
constellation of symptoms is adequate for diagnosis without chest imaging. For example, the
positive predictive value of the combination of fever, tachycardia, rales, and hypoxia (oxygen
saturation <95 percent) among patients with respiratory complaints presenting to primary
care was <60 percent when chest radiograph was used as a reference standard [24].
Signs and symptoms of pneumonia can also be subtle in patients with advanced age and/or
impaired immune systems, and a higher degree of suspicion may be needed to make the
diagnosis. As examples, older patients may present with mental status changes but lack fever
or leukocytosis [25]. In immunocompromised patients, pulmonary infiltrates may not be
detectable on chest radiographs but can be visualized with computed tomography.
The clinical and diagnostic features of CAP and sepsis are discussed in detail separately. (See
"Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and
"Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and
prognosis", section on 'Clinical presentation'.)
DIAGNOSIS
Making the diagnosis — The diagnosis of CAP generally requires the demonstration of an

infiltrate on chest imaging in a patient with a clinically compatible syndrome (eg, fever,
dyspnea, cough, and sputum production) [26].
● For most patients with suspected CAP, we obtain posteroanterior and lateral chest
radiographs. Radiographic findings consistent with the diagnosis of CAP include lobar
consolidations ( image 1C), interstitial infiltrates ( image 1D-E), and/or cavitations
( image 2). Although certain radiographic features suggest certain causes of
pneumonia (eg, lobar consolidations suggest infection with typical bacterial pathogens),
radiographic appearance alone cannot reliably differentiate among etiologies.
● For selected patients in whom CAP is suspected based on clinical features despite a
negative chest radiograph, we obtain computed tomography (CT) of the chest. These
patients include immunocompromised patients, who may not mount strong
inflammatory responses and thus have negative chest radiographs, as well as patients
with known exposures to epidemic pathogens that cause pneumonia (eg, Legionella).
Because there is no direct evidence to suggest that CT scanning improves outcomes for
most patients and cost is high, we do not routinely obtain CT scans when evaluating
patients for CAP.
The combination of a compatible clinical syndrome and imaging findings consistent with
pneumonia are sufficient to establish an initial clinical diagnosis of CAP. However, this
combination of findings is nonspecific and is shared among many cardiopulmonary disorders.
Thus, remaining attentive to the possibility of an alternate diagnosis as a patient's course
evolves is important to care. (See 'Differential diagnosis' below.)
Defining severity and site of care — For patients with a working diagnosis of CAP, the next
steps in management are defining the severity of illness and determining the most
appropriate site of care. Determining the severity of illness is based on clinical judgement and
can be supplemented by use of severity scores ( algorithm 1).
The most commonly used severity scores are the Pneumonia Severity Index (PSI) and CURB-65
[27,28]. We generally prefer the PSI, also known as the PORT score (calculator 1), because it is
the most accurate and its safety and effectiveness in guiding clinical decision-making have
been validated [29-32]. However, the CURB-65 score is a reasonable alternative and is preferred
by many clinicians because it is easier to use (calculator 2).
The three levels of severity (mild, moderate, and severe) generally correspond to three levels
of care:
● Ambulatory care – Most patients who are otherwise healthy with normal vital signs
(apart from fever) and no concern for complication are considered to have mild
pneumonia and can be managed in the ambulatory setting. These patients typically have
PSI scores of I to II and CURB-65 scores of 0 (or a CURB-65 score of 1 if age >65 years).
● Hospital admission – Patients who have peripheral oxygen saturations <92 percent on
room air (and a significant change from baseline) should be hospitalized. In addition,
patients with PSI scores of ≥III and CURB-65 scores ≥1 (or CURB-65 score ≥2 if age >65
years) should also generally be hospitalized.
Because patients with early signs of sepsis, rapidly progressive illness, or suspected
infections with aggressive pathogens are not well represented in severity scoring
systems, these patients may also warrant hospitalization in order to closely monitor the
response to treatment.
Practical concerns that may warrant hospital admission include an inability to take oral
medications, cognitive or functional impairment, or other social issues that could impair
medication adherence or ability to return to care for clinical worsening (eg, substance
abuse, homelessness, or residence far from a medical facility).
● Intensive care unit (ICU) admission – Patients who meet either of the following major
criteria have severe CAP and should be admitted to the ICU [26]:
• Respiratory failure requiring mechanical ventilation

• Sepsis requiring vasopressor support
Recognizing these two criteria for ICU admission is relatively straightforward. The
challenge is to identify patients with severe CAP who have progressed to sepsis before
the development of organ failure. For these patients, early ICU admission and
administration of appropriate antibiotics improve outcomes. To help identify patients
with severe CAP before development of organ failure, the American Thoracic Society (ATS)
and the Infectious Diseases Society of America (IDSA) suggest minor criteria [1,26].
The presence of three of these criteria warrants ICU admission:
• Altered mental status

• Hypotension requiring fluid support
• Temperature <36°C (96.8°F)
• Respiratory rate ≥30 breaths/minute
• Arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) ratio ≤250
• Blood urea nitrogen (BUN) ≥20 mg/dL (7 mmol/L)

• Leukocyte count <4000 cells/microL
• Platelet count <100,000/mL
• Multilobar infiltrates
Although several other scores for identifying patients with severe CAP and/or ICU admission
have been developed, we generally use the ATS/IDSA major and minor criteria because they
are well validated [33-35].
Detailed discussion on assessing severity and determining the site of care in patients with CAP
is provided separately. (See "Community-acquired pneumonia in adults: Assessing severity and
determining the appropriate site of care".)
Triage of patients with known or suspected COVID-19 is also discussed elsewhere. (See
"COVID-19: Evaluation of adults with acute illness in the outpatient setting", section on
'Determine if in-person evaluation warranted'.)
Microbiologic testing — The benefit of obtaining a microbiologic diagnosis should be

balanced against the time and cost associated with an extensive evaluation in each patient.
Generally, we take a tiered approach to microbiologic evaluation based on CAP severity and
the site of care ( table 5):
● Outpatients − For most patients with mild CAP being treated in the ambulatory setting,
microbiologic testing is not needed (apart from testing for SARS-CoV-2 during the
pandemic). Empiric antibiotic therapy is generally successful, and knowledge of the
infecting pathogen does not usually improve outcomes.
● Patients with moderate CAP admitted to the general medicine ward − For most
patients with moderate CAP admitted to the general medical ward, we obtain the
following:
• Blood cultures
• Sputum Gram stain and culture
• Urinary antigen testing for S. pneumoniae
• Testing for Legionella spp (polymerase chain reaction [PCR] when available, urinary
antigen test as an alternate)
• SARS-CoV-2 testing
During the pandemic, we test all patients for COVID-19. During respiratory virus season
(eg, late fall to early spring in the northern hemisphere), we also test for other
respiratory viruses (eg, influenza, adenovirus, parainfluenza, respiratory syncytial virus,

and human metapneumovirus). When testing for influenza, PCR is preferred over rapid
antigen testing. (See "Seasonal influenza in adults: Clinical manifestations and
diagnosis".)
For these patients, making a microbiologic diagnosis allows for directed therapy, which
helps limit antibiotic overuse, prevent antimicrobial resistance, and reduce unnecessary
complications, such as Clostridioides difficile infections.
● Patients with severe CAP (including ICU admission) − For most hospitalized patients
with severe CAP, including those admitted to the ICU, we send blood cultures, sputum
cultures, urinary streptococcal antigen, and Legionella testing. In addition, we obtain
bronchoscopic specimens for microbiologic testing when feasible, weighing the benefits
of obtaining a microbiologic diagnosis against the risks of the procedure (eg, need for
intubation, bleeding, bronchospasm, pneumothorax) on a case-by-case basis. When
pursuing bronchoscopy, we usually send specimens for aerobic culture, Legionella
culture, fungal stain and culture, and testing for respiratory viruses.
The type of viral diagnostic tests used (eg, PCR, serology, culture) vary among institutions.
In some cases, multiplex PCR panels that test for a wide array of viral and bacterial
pathogens are used. While we generally favor using these tests for patients with severe
pneumonia, we interpret results with caution as most multiplex assays have not been
approved for use on lower respiratory tract specimens. In particular, the detection of
single viral pathogen does not confirm the diagnosis of viral pneumonia because viruses
can serve as cofactors in the pathogenesis of bacterial CAP or can be harbored
asymptomatically.
In all cases, we modify this approach based on epidemiologic exposures, patient risk factors,
and clinical features regardless of CAP severity or treatment setting ( table 3). As examples:
● For patients with known or probable exposures to epidemic pathogens such as Legionella
or epidemic coronaviruses, we broaden our evaluation to include tests for these
pathogens. (See "Clinical evaluation and diagnostic testing for community-acquired
pneumonia in adults", section on 'Important pathogens'.)
● For patients with cavitary pneumonia, we may include testing for tuberculosis, fungal
pathogens, and Nocardia.
● For immunocompromised patients, we broaden our differential to include opportunistic

pathogens such as Pneumocystis jirovecii, fungal pathogens, parasites, and less common
viral pathogens such as cytomegalovirus. The approach to diagnostic testing varies

based on the type and degree of immunosuppression and other patient-specific factors.
(See "Approach to the immunocompromised patient with fever and pulmonary
infiltrates" and "Epidemiology of pulmonary infections in immunocompromised
patients".)
When defining the scope of our microbiologic evaluation, we also take the certainty of the
diagnosis of CAP into consideration. Because a substantial portion of patients hospitalized
with an initial clinical diagnosis of CAP are ultimately found to have alternate diagnoses [17],
pursuing a comprehensive microbiologic evaluation can help reach the final diagnosis (eg,
blood cultures obtained as part of the evaluation for CAP may help lead to a final diagnosis of
endocarditis).
Detailed discussion on the microbiologic evaluation of CAP is provided separately. (See "Clinical
evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Sputum
cultures for the evaluation of bacterial pneumonia".)
The diagnosis of COVID-19 during the pandemic is also discussed in detail elsewhere. (See
"COVID-19: Diagnosis".)
DIFFERENTIAL DIAGNOSIS
CAP is a common working diagnosis and is frequently on the differential diagnosis of patients
presenting with a pulmonary infiltrate and cough, patients with respiratory tract infections,
and patients with sepsis. (See "Clinical evaluation and diagnostic testing for community-
acquired pneumonia in adults", section on 'Differential diagnosis'.)
Noninfectious illnesses that mimic CAP or co-occur with CAP and present with pulmonary
infiltrate and cough include:
• Congestive heart failure with pulmonary edema

• Pulmonary embolism
• Pulmonary hemorrhage
• Atelectasis
• Aspiration or chemical pneumonitis
• Drug reactions
• Lung cancer
• Collagen vascular diseases
• Vasculitis
• Acute exacerbation of bronchiectasis

• Interstitial lung diseases (eg, sarcoidosis, asbestosis, hypersensitivity pneumonitis,
cryptogenic organizing pneumonia)
For patients with an initial clinical diagnosis of CAP who have rapidly resolving pulmonary
infiltrates, alternate diagnoses should be investigated. Pulmonary infiltrates in CAP are
primarily caused by the accumulation of white blood cells (WBCs) in the alveolar space and
typically take weeks to resolve. A pulmonary infiltrate that resolves in one or two days may be
caused by accumulation of fluid in the alveoli (ie, pulmonary edema) or a collapse of the alveoli
(ie, atelectasis) but not due to accumulation of WBCs.
Respiratory illnesses that mimic CAP or co-occur with CAP include:
• Acute exacerbations of chronic obstructive pulmonary disease

• Influenza and other respiratory viral infections
• Acute bronchitis ( figure 4)
• Asthma exacerbations
Febrile illness and/or sepsis can also be the presenting syndrome in patients with CAP; other
common causes of these syndromes include urinary tract infections, intraabdominal
infections, and endocarditis.
TREATMENT
For most patients with CAP and excluding COVID-19, the etiology is not known at the time of
diagnosis, and antibiotic treatment is empiric, targeting the most likely pathogens. The
pathogens most likely to cause CAP vary with severity of illness, local epidemiology, and patient
risk factors for infection with drug-resistant organisms.
As an example, for most patients with mild CAP who are otherwise healthy and treated in the
ambulatory setting, the range of potential pathogens is limited. By contrast, for patients with
CAP severe enough to require hospitalization, potential pathogens are more diverse, and the
initial treatment regimens are often broader.
The management of COVID-19 is discussed in detail elsewhere. (See "COVID-19: Management

in hospitalized adults" and "COVID-19: Management in nursing homes" and "COVID-19:
Management of adults with acute illness in the outpatient setting".)
Outpatient antibiotic therapy — For all patients with CAP, empiric regimens are designed to
target S. pneumoniae (the most common and virulent bacterial CAP pathogen) and atypical
pathogens. Coverage is expanded for outpatients with comorbidities, smoking, and recent
antibiotic use to include or better treat beta-lactamase-producing H. influenzae, M. catarrhalis,
and methicillin-susceptible S. aureus. For those with structural lung disease, we further expand
coverage to include Enterobacteriaceae, such as E. coli and Klebsiella spp ( algorithm 2).
Selection of the initial regimen depends on the adverse effect profiles of available agents,
potential drug interactions, patient allergies, and other patient-specific factors.
● For most patients aged <65 years who are otherwise healthy and have not recently used
antibiotics, we typically use oral amoxicillin (1 g three times daily) plus a macrolide (eg,
azithromycin or clarithromycin) or doxycycline. Generally, we prefer to use a macrolide
over doxycycline.
This approach differs from the American Thoracic Society (ATS)/Infectious Diseases
Society of America (IDSA), which recommend monotherapy with amoxicillin as first line
and monotherapy with either doxycycline or a macrolide (if local resistance rates are <25
percent [eg, not in the United States]) as alternatives for this population [26]. The
rationale for each approach is discussed separately. (See "Treatment of community-
acquired pneumonia in adults in the outpatient setting", section on 'Empiric antibiotic
treatment'.)
● For patients who have major comorbidities (eg, chronic heart, lung, kidney, or liver
disease, diabetes mellitus, alcohol dependence, or immunosuppression), who are
smokers, and/or who have used antibiotics within the past three months, we suggest
oral amoxicillin-clavulanate (875 mg twice daily or extended release 2 g twice daily) plus
either a macrolide (preferred) or doxycycline.
Alternatives to amoxicillin-based regimens include combination therapy with a cephalosporin

plus a macrolide or doxycycline or monotherapy with lefamulin.
● For patients who can use cephalosporins, we use a third-generation cephalosporin (eg,
cefpodoxime) plus either a macrolide or doxycycline.
● For patients who cannot use any beta-lactam, we select a respiratory fluoroquinolone
(eg, levofloxacin, moxifloxacin, gemifloxacin) or lefamulin. For those with structural lung
disease, we prefer a respiratory fluoroquinolone because its spectrum of activity includes
Enterobacteriaceae.
In the absence of hepatic impairment or drug interactions, lefamulin is a potential

alternative to fluoroquinolones for most others. However, clinical experience with this
agent is limited. Use should be avoided in patients with moderate to severe hepatic
dysfunction, known long QT syndrome, or in those taking QT-prolonging agents,
pregnant and breastfeeding women, and women with reproductive potential not using
contraception. There are drug interactions with CYP3A4 and P-gp inducers and
substrates; in addition, lefamulin tablets are contraindicated with QT-prolonging CYP3A4
substrates. Refer to the Lexicomp drug interactions tool included within UpToDate.
Omadacycline is another newer agent that is active against most CAP pathogens,
including Enterobacteriaceae. It is a potential alternative for patients who cannot tolerate
beta-lactams (or other agents) and want to avoid fluoroquinolones. (See "Treatment of
community-acquired pneumonia in adults who require hospitalization", section on 'New
antimicrobial agents'.)
Modifications to these regimens may be needed for antibiotic allergy, drug interactions,
specific exposures, and other patient-specific factors. In particular, during influenza season,
patients at high risk for poor outcomes from influenza may warrant antiviral therapy
( table 6).
We treat most patients for five days. However, we generally ensure that all patients are
improving on therapy and are afebrile for at least 48 hours before stopping antibiotics. In
general, extending the treatment course beyond seven days does not add benefit. Studies
supporting this approach are discussed separately. (See "Treatment of community-acquired
pneumonia in adults in the outpatient setting", section on 'Duration of therapy'.)
Detailed discussion on the treatment of CAP in the outpatient setting, including antibiotic
efficacy data, is provided separately. (See "Treatment of community-acquired pneumonia in
adults in the outpatient setting".)
Inpatient antibiotic therapy
General medical ward — For patients with CAP admitted to the medical ward, empiric
antibiotic regimens are designed to treat S. aureus, gram-negative enteric bacilli (eg, Klebsiella
pneumoniae) in addition to typical pathogens (eg, S. pneumoniae, H. influenzae, and M. catarrhalis)
and atypical pathogens (eg, Legionella pneumophilia, M. pneumoniae, and C. pneumoniae).
We generally start antibiotic therapy as soon as we are confident that CAP is the appropriate
working diagnosis and, ideally, within four hours of presentation. Delays in appropriate
antibiotic treatment that exceed four hours have been associated with increased mortality
[36].
The key factors in selecting an initial regimen for hospitalized patients with CAP are risk of
infection with Pseudomonas and/or methicillin-resistant S. aureus (MRSA). The strongest risk
factors for MRSA or Pseudomonas infection are known colonization or prior infection with
these organisms, particularly from a respiratory tract specimen. Recent hospitalization (ie,
within the past three months) with receipt of intravenous (IV) antibiotics is also a risk factor,
particularly for pseudomonal infection. Suspicion for these pathogens should otherwise be
based on local prevalence (when known), other patient-specific risk factors, and the overall
clinical assessment ( algorithm 3 and table 4):
● For patients without suspicion for MRSA or Pseudomonas, we generally use one of two
regimens: combination therapy with a beta-lactam plus a macrolide or monotherapy with
a respiratory fluoroquinolone [26]. Because these two regimens have similar clinical
efficacy, we select among them based on other factors (eg, antibiotic allergy, drug
interactions). For patients who are unable to use either a macrolide or a fluoroquinolone,
we use a beta-lactam plus doxycycline.
● For patients with known colonization or prior infection with Pseudomonas, recent
hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal
infection, we typically use combination therapy with both an antipseudomonal beta-
lactam (eg, piperacillin-tazobactam, cefepime, ceftazidime, meropenem, or imipenem)
plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin). The
selection of empiric regimens should also be informed by the susceptibility pattern for
prior isolates.
● For patients with known colonization or prior infection with MRSA or other strong
suspicion for MRSA infection, we add an agent with anti-MRSA activity, such as
vancomycin or linezolid, to either of the above regimens. We generally prefer linezolid
over vancomycin when community-acquired MRSA is suspected (eg, a young, otherwise
healthy patient who plays contact sports presenting with necrotizing pneumonia)
because of linezolid's ability to inhibit bacterial toxin production [37]. Ceftaroline is a
potential alternative for the treatment of MRSA pneumonia but is not US Food and Drug
Administration approved. (See "Treatment of community-acquired pneumonia in adults
who require hospitalization", section on 'Community-acquired MRSA'.)
Modifications to initial empiric regimens may be needed for antibiotic allergy, potential drug
interactions, current epidemics, specific exposures, resistance patterns of known colonizing
organisms or organisms isolated during prior infections, and other patient-specific factors. In
particular, antiviral treatment (eg, oseltamivir) should be given as soon as possible for any
hospitalized patient with known or suspected influenza. (See "Seasonal influenza in

nonpregnant adults: Treatment".)
Detailed discussion about antibiotic therapy, including use of new agents (eg, lefamulin,
omadacycline) for patients hospitalized to a general medical ward is provided separately. (See
"Treatment of community-acquired pneumonia in adults who require hospitalization".)
ICU admission
Antibiotic selection — For patients with CAP admitted to the intensive care unit (ICU),
our approach to antibiotic selection is similar to that used for patients admitted to the general
medical ward. However, because of the severity of illness in this population, we do not use
monotherapy ( algorithm 4). In addition, we start antibiotic therapy within one hour of
presentation for patients who are critically ill.
The spectrum of activity of the empiric regimen should be broadened in patients with risk
factors for Pseudomonas infection or MRSA infection ( table 4).
● For most patients without suspicion for MRSA or Pseudomonas, we treat with a beta-
lactam (eg, ceftriaxone, cefotaxime, ceftaroline, ampicillin-sulbactam, ertapenem) plus a
macrolide (eg, azithromycin or clarithromycin) or a beta-lactam plus a respiratory
fluoroquinolone (eg, levofloxacin or moxifloxacin) [26].
For patients with penicillin hypersensitivity reactions, we select an appropriate agent (eg,
later-generation cephalosporin, carbapenem, or a beta-lactam alternative) based on the
type and severity of reaction ( algorithm 5). For patients who cannot use any beta-
lactam (ie, penicillins, cephalosporins, and carbapenems), we typically use combination
therapy with a respiratory fluoroquinolone and aztreonam.
● For patients with known colonization or prior infection with MRSA, recent
hospitalization with IV antibiotic use, or other strong suspicion for MRSA infection,
we add an agent with anti-MRSA activity, such as vancomycin or linezolid, to either of the
above regimens [26].
● For patients with known colonization or prior infection with Pseudomonas, recent
hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal
infection, we typically use combination therapy with both an antipseudomonal beta-
lactam (eg, piperacillin-tazobactam, cefepime, ceftazidime, meropenem, or imipenem)
plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin) for empiric
treatment [26].
For patients with penicillin hypersensitivity reactions, we select an appropriate agent

based on the type and severity of penicillin reaction ( algorithm 5) and prior
pseudomonal susceptibility testing.
Modifications to initial empiric regimens may be needed for antibiotic allergy, potential drug
interactions, current epidemics, specific exposures, resistance patterns of colonizing bacteria
or bacteria isolated during prior infections, and other patient-specific factors. In particular,
antiviral treatment (eg, oseltamivir) should be given as soon as possible for any hospitalized
patient with known or suspected influenza. (See "Seasonal influenza in nonpregnant adults:
Treatment".)
Detailed discussion about antibiotic treatment for patients with CAP admitted to the ICU and
patients with sepsis and/or respiratory failure are provided separately. (See "Treatment of
community-acquired pneumonia in adults who require hospitalization", section on 'Intensive
care unit' and "Evaluation and management of suspected sepsis and septic shock in adults".)
Adjunctive glucocorticoids — The use of glucocorticoids as an adjunctive treatment for

CAP is controversial, and we, along with the ATS/IDSA, do not recommend routine use for most
patients with CAP [26,38,39]. The rationale for treating patients with CAP with glucocorticoids is
to reduce the dysregulated systemic inflammatory response, which contributes to morbidity
and mortality. However, the population that may benefit most from this intervention is not
well-defined, and adverse effects are potentially severe.
● We suggest giving adjunctive glucocorticoids to patients with CAP who have evidence of
an exaggerated or dysregulated host inflammatory response, defined as septic shock
that is refractory to fluid resuscitation and vasopressor administration or respiratory
failure with a fraction of inspired oxygen requirement of >50 percent plus one or more of
the following criteria: metabolic acidosis with an arterial pH of <7.3, lactate >4 mmol/L, or
a C-reactive protein >150 mg/L.
● When using adjunctive glucocorticoids, we treat for five days. For patients who are
unable to take oral medications, we use methylprednisolone 0.5 mg/kg IV every 12 hours.
For patients who can take oral medications, we use prednisone 50 mg orally daily. We do
not use adjunctive glucocorticoids in patients with influenza or in patients at risk of
aspergillosis.
The use of glucocorticoids in severe CAP is discussed in detail separately. There is limited role
for the use of glucocorticoids for the treatment of CAP in patients who are not critically ill. (See
"Treatment of community-acquired pneumonia in adults who require hospitalization", section
on 'Adjunctive glucocorticoids'.)
Use of glucocorticoids for patients with COVID-19 is discussed elsewhere. (See "COVID-19:
Management in hospitalized adults", section on 'Dexamethasone and other glucocorticoids'.)
Disposition — Once a patient with CAP is hospitalized, further management will be dictated

by the patient's response to initial empiric therapy. Clinical response should be assessed
during daily rounds. While various criteria have been proposed to assess clinical response [40-
42], we generally look for subjective improvement in cough, sputum production, dyspnea, and
chest pain. Objectively, we assess for resolution of fever and normalization of heart rate,
respiratory rate, oxygenation, and white blood cell count. Generally, patients demonstrate
some clinical improvement within 48 to 72 hours ( table 7).
Antibiotic de-escalation — For patients in whom a causative pathogen has been

identified, we tailor therapy to target the pathogen [43]. If coverage for MRSA was added
empirically, and MRSA was not identified as a pathogen nor on a screening nasal swab and the
patient is improving, we typically discontinue the anti-MRSA agent (eg, vancomycin). However,
for the majority of patients hospitalized with CAP, a causative pathogen is not identified. For
these patients, we continue empiric treatment for the duration of therapy, provided that the
patient is improving. Intravenous antibiotic regimens can be transitioned to oral regimens
with a similar spectrum activity as the patient improves ( algorithm 6) [44,45].
Duration of therapy — We generally determine the duration of therapy based on the

patient's clinical response to therapy.
For all patients, we treat until the patient has been afebrile and clinically stable for at least 48
hours and for a minimum of five days. Patients with mild infection generally require five to
seven days of therapy. Patients with severe infection or chronic comorbidities generally
require 7 to 10 days of therapy. Extended courses may be needed for immunocompromised
patients, patients with infections caused by certain pathogens (eg, P. aeruginosa), or those with
complications. (See "Treatment of community-acquired pneumonia in adults who require
hospitalization", section on 'Duration of therapy'.)
In accord with the ATS/IDSA, we do not use procalcitonin to help determine whether to start
antibiotics [26]. However, we sometimes use procalcitonin thresholds as an adjunct to clinical
judgment to help guide antibiotic discontinuation in clinically stable patients. We generally
obtain a level at the time of diagnosis and repeat the level every one to two days in patients
who are clinically stable. We determine the need for continued antibiotic therapy based on
clinical improvement and serial procalcitonin levels ( algorithm 7). (See "Procalcitonin use in
lower respiratory tract infections".)
Discharge — Hospital discharge is appropriate when the patient is clinically stable, can

take oral medication, has no other active medical problems, and has a safe environment for
continued care. Patients do not need to be kept overnight for observation following the switch
to oral therapy. Early discharge based on clinical stability and criteria for switching to oral
therapy is encouraged to reduce risk associated with prolonged hospital stays and
unnecessary cost.
Immunocompromised patients — The spectrum of potential pathogens expands

considerably in immunocompromised patients to include invasive fungal infections, less
common viral infections (eg, cytomegalovirus), and parasitic infections (eg, toxoplasmosis)
[46].
The risk for specific infections varies with the type and degree of immunosuppression and
whether the patient is taking prophylactic antimicrobials. As examples, prolonged
neutropenia, T cell immunosuppression, and use of tumor necrosis factor-alpha inhibitors
predispose to invasive fungal infections (eg, aspergillosis, mucormycosis) as well as
mycobacterial infections. Advanced human immunodeficiency virus (HIV) infection (eg, CD4 cell
count <200 cells/microL), prolonged glucocorticoid use (particularly when used with certain
chemotherapeutics), and lymphopenia each should raise suspicion for pneumocystis
pneumonia. Multiple infections may occur concurrently in this population, and the likelihood
of disseminated infection is greater. Because signs and symptoms of infection can be subtle
and nonspecific in immunocompromised patients, diagnosis can be challenging and invasive
procedures are often required for microbiologic diagnosis. Broad-spectrum empiric therapy
may be needed prior to obtaining a specific microbiologic diagnosis.
Because management is complex, drug interactions are common, adjustments in

immunosuppressive regimens may be needed, and empiric treatment options (eg,
amphotericin B) can be associated with significant toxicity, we generally involve a
multidisciplinary team of specialists when caring for immunocompromised patients with
pneumonia. (See "Epidemiology of pulmonary infections in immunocompromised patients"
and "Approach to the immunocompromised patient with fever and pulmonary infiltrates" and
"Tumor necrosis factor-alpha inhibitors: Bacterial, viral, and fungal infections".)
FOLLOW-UP IMAGING
Most patients with clinical resolution after treatment do not require a follow-up chest
radiograph, as radiographic response lags behind clinical response. However, follow-up clinic
visits are good opportunities to review the patient's risk for lung cancer based on age,
smoking history, and recent imaging findings ( algorithm 8).
This approach is similar to that outlined by the ATS/IDSA, which recommend not obtaining a
follow-up chest radiograph in patients whose symptoms have resolved within five to seven
days [26]. (See "Treatment of community-acquired pneumonia in adults who require
hospitalization", section on 'Follow-up chest radiograph'.)
COMPLICATIONS AND PROGNOSIS
While most patients with CAP will recover with appropriate antibiotic treatment, some will
progress and/or develop complications despite appropriate therapy (ie, clinical failure) and
some will remain symptomatic (ie, nonresolving pneumonia).
Clinical failure — Clear indicators of clinical failure include progression to sepsis and/or

respiratory failure despite appropriate antibiotic treatment and respiratory support. Other
indicators include an increase in subjective symptoms (eg, cough, dyspnea) usually in
combination with objective criteria (eg, decline in oxygenation, persistent fever, or rising white
blood cell). Various criteria have been proposed to define clinical failure but none widely
adopted [47-49].
Reasons for clinical failure generally fall into these categories:
● Progression of the initial infection – For some patients, CAP can lead to overwhelming
infection despite appropriate antibiotic treatment. In some, this indicates a dysregulated
host immune response. In others, this may indicate that the infection has spread beyond
the pulmonary parenchyma (eg, empyema, lung abscess, bacteremia, endocarditis).
Other possibilities include infection with a drug-resistant pathogen or an unusual

pathogen not covered by the initial empiric antibiotic regimen. Alternatively, failure to
respond to treatment may signify the presence of an immunodeficiency (eg, new
diagnosis of HIV infection).
● Development of comorbid complications – Comorbid complications may be infectious

or noninfectious. Nosocomial infections, particularly hospital-acquired pneumonia (HAP),
are common causes of clinical failure. In addition to HAP, others include catheter-related
bloodstream infections, urinary tract infections, and C. difficile infection [50].
Cardiovascular events are also common complications and include acute myocardial
infarction, cardiac arrhythmias, congestive heart failure, pulmonary embolism, and
stroke [51-53]. Older age, preexisting cardiovascular disease, severe pneumonia, and
infection with certain pathogens (ie, S. pneumoniae and influenza) have each been
associated with increased risk of cardiovascular events [51,54-56]. Recognition that
cardiovascular events and other systemic complications can occur during the acute
phase of CAP is also changing our view of CAP from an acute pulmonary process to an
acute systemic disease. (See "Morbidity and mortality associated with community-
acquired pneumonia in adults", section on 'Cardiac complications'.)
Because of these possibilities, we generally broaden our initial antibiotic regimen for patients
who are progressing despite appropriate empiric treatment and evaluate for alternate
diagnoses, less common or drug-resistant pathogens, and/or infectious and cardiovascular
complications. (See 'Differential diagnosis' above and "Morbidity and mortality associated with
community-acquired pneumonia in adults".)
Nonresolving CAP — For some patients, initial symptoms will neither progress nor improve
with at least seven days of appropriate empiric antibiotic treatment. We generally characterize
these patients as having nonresolving pneumonia. Potential causes of nonresolving CAP
include:
● Delayed clinical response – For some patients, particularly those with multiple
comorbidities, severe pneumonia, bacteremia, and infection with certain pathogens (eg,
S. pneumoniae), treatment response may be slow. Eight or nine days of treatment may be
needed before clinical improvement is evident.
● Loculated infection – Patients with complications such as lung abscess, empyema, or

other closed space infections may fail to improve clinically despite appropriate antibiotic
selection. Such infections may require drainage and/or prolonged antibiotic treatment.
(See "Lung abscess in adults" and "Epidemiology, clinical presentation, and diagnostic
evaluation of parapneumonic effusion and empyema in adults".)
● Bronchial obstruction – Bronchial obstruction (eg, by a tumor) can cause a

postobstructive pneumonia that may fail to respond or slowly respond to standard
empiric antibiotic regimens for CAP.
● Pathogens that cause subacute/chronic CAP – Mycobacterium tuberculosis,

nontuberculous mycobacteria (eg, Mycobacterium kansasii), fungi (eg, Histoplasma
capsulatum, Blastomyces dermatitidis), or less common bacteria (eg, Nocardia spp,
Actinomyces israelii) can cause subacute or chronic pneumonia that may fail to respond or
may incompletely respond to standard empiric antibiotic regimens for CAP.
● Incorrect initial diagnosis – Failure to improve despite seven days of treatment also
raises the possibility of an alternate diagnosis (eg, malignancy or inflammatory lung
disease). (See 'Differential diagnosis' above.)
Once a patient is characterized as having nonresolving CAP, a complete new physical

examination, laboratory evaluation, imaging studies, and microbiologic workup will be
necessary to define the etiology of nonresolving CAP [50]. Initiation of workup for
nonresolving CAP should not be automatically associated with a change in initial empiric
antibiotic therapy. (See "Nonresolving pneumonia".)
Long-term complications and mortality — Although the majority of patient with CAP recover
without complications, CAP is a severe illness and among the leading causes of mortality
worldwide. Mortality can be directly attributable to CAP (eg, overwhelming sepsis or
respiratory failure) or can result indirectly from cardiovascular events or other comorbid
complications (eg, advanced chronic obstructive pulmonary disease [COPD]) [57].
Long-term complications resulting from pneumonia are increasingly recognized and there is a
shift in the medical community to define pneumonia as a systemic illness that can lead to
chronic disease [58]. While the precise incidence of long-term complications is not known, the
more common long-term sequelae involve the respiratory tract and cardiovascular system
[59].
In the United States, pneumonia (combined with influenza) is among the top 10 most common
causes of death [5]. Thirty-day mortality rates vary with disease severity, ranging from less
than 1 percent in ambulatory patients to approximately 20 to 25 percent in patients with
severe CAP. In addition to disease severity, older age, comorbidities (eg, COPD, diabetes
mellitus, cardiovascular disease), infection with certain pathogens (eg, S. pneumoniae), and
acute cardiac complications are each associated with increased short-term mortality [51,60,61].
CAP is also associated with increased long-term mortality [7,62-64]. In one population-based
study evaluating 7449 patients hospitalized with CAP, mortality rates were 6.5 percent during
hospitalization, 13 percent 30 days after hospitalization, 23 percent at six months after
hospitalization, and 31 percent at one year after hospitalization [7]. During the same study
year, an estimated 1,581,860 patients were hospitalized in the United States. Extrapolating
mortality data to these patients, the number of deaths in the United States population will be
102,821 during hospitalization, 205,642 at 30 days, 370,156 at six months, and 484,050 at one
year [7]. Causes of long-term mortality are primarily related to comorbidities and include
malignancy, COPD, and cardiovascular disease [57].
Data associating CAP with long-term mortality indicate that CAP is not only a common cause of
acute morbidity and mortality but also a disease with important chronic health outcomes.
PREVENTION
The three primary pillars for the prevention of CAP are [65-67]:
● Smoking cessation (when appropriate)

● Influenza vaccination for all patients
● Pneumococcal vaccination for at-risk patients
Each is discussed in detail separately. (See "Overview of smoking cessation management in

adults" and "Seasonal influenza vaccination in adults" and "Pneumococcal vaccination in
adults".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Community-acquired
pneumonia in adults".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have about
a given condition. These articles are best for patients who want a general overview and who
prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer,
more sophisticated, and more detailed. These articles are written at the 10th to 12th grade
reading level and are best for patients who want in-depth information and are comfortable
with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or email these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topic (see "Patient education: Pneumonia in adults (The Basics)")
● Beyond the Basics topic (see "Patient education: Pneumonia in adults (Beyond the
Basics)")
SUMMARY AND RECOMMENDATIONS
● Background − Community-acquired pneumonia (CAP) is a leading cause of morbidity and

mortality worldwide. (See 'Incidence' above.)
● Risk factors − Risk factors include age ≥65 years, chronic comorbidities, concurrent or
antecedent respiratory viral infections, impaired airway protection, smoking, alcohol
abuse, and other lifestyle factors (eg, crowded living conditions). (See 'Risk factors'
above.)
● Microbiology − The most commonly identified causes of CAP include respiratory viruses
(particularly severe acute respiratory syndrome coronavirus 2 during the pandemic),
typical bacteria (eg, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis)
and atypical bacteria (eg, Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae).
Pseudomonas and methicillin-resistant Staphylococcus aureus (MRSA) are less common
causes that predominantly occur in patients with specific risk factors. (See 'Microbiology'
above and 'Pathogenesis' above.)
● Making the diagnosis − Diagnosis requires demonstration of an infiltrate on chest

imaging in a patient with a clinically compatible syndrome (eg, fever, dyspnea, cough, and
leukocytosis). For most patients, a posteroanterior and lateral chest radiograph is
sufficient. Computed tomography scan is reserved for selected cases. (See 'Clinical
presentation' above and 'Making the diagnosis' above.)
● Alternate and concurrent diagnoses − While the combination of a compatible clinical

syndrome and an infiltrate on chest imaging are sufficient to establish an initial clinical
diagnosis of CAP, these findings are nonspecific. Remaining attentive to the possibility of
an alternate or concurrent diagnosis as a patient's course evolves is important to care.
(See 'Differential diagnosis' above.)
● Determining severity of illness − For patients with a working diagnosis of CAP, the initial
steps in management are defining the severity of illness and determining the most
appropriate site of care ( algorithm 1). For most patients, we determine our approach
to microbiologic testing based on this assessment ( table 5). (See 'Microbiologic
testing' above.)
● Empiric antibiotic selection − The selection of an empiric antibiotic regimen is based on

the severity of illness, site of care, and most likely pathogens. We generally start
antibiotics as soon as we are confident that CAP is the appropriate working diagnosis
and, ideally, within four hours of presentation for inpatients and within one hour of
presentation for those who are critically ill (see 'Treatment' above):
• For most outpatients, we prefer to use combination therapy with a beta-lactam and
either a macrolide (preferred) or doxycycline. Alternatives to beta-lactam-based
regimens include monotherapy with either a fluoroquinolone or, alternatively,
lefamulin or omadacycline (newer agents). Selection among these agents depends on
patient comorbidities, drug interactions, allergies, and other intolerances. Clinical
experience with lefamulin and omadacycline are limited; warnings and
contraindications exist ( algorithm 2).
This approach differs from the American Thoracic Society/Infectious Diseases Society
of America, which recommend monotherapy with amoxicillin as first line and
monotherapy with either doxycycline or a macrolide (if local resistance rates are <25
percent [eg, not in the United States]) as alternatives for this population.
• For most inpatients admitted to the general medical ward, treatment options include
either intravenous (IV) combination therapy with a beta-lactam plus a macrolide or
doxycycline or monotherapy with a respiratory fluoroquinolone ( algorithm 3).
These regimens should be expanded for patients with risk factors for Pseudomonas or
MRSA ( table 4).
• For most patients admitted to the intensive care unit (ICU), treatment options include
IV combination therapy with a beta-lactam plus either a macrolide or a respiratory
fluoroquinolone ( algorithm 4). As with other hospitalized patients, regimens should
be expanded for patients with risk factors for Pseudomonas or MRSA ( table 4).
● Directed therapy − For patients in whom a causative pathogen has been identified, we
tailor therapy to target the pathogen. (See 'Antibiotic de-escalation' above.)
● Duration of antibiotics − For all patients, we treat until the patient has been afebrile and
clinically stable for at least 48 hours and for a minimum of five days. Patients with mild
infection generally require five to seven days of therapy; those with severe infection or
chronic comorbidities generally require 7 to 10 days of therapy. (See 'Duration of therapy'
above.)
● Lack of response to antibiotics − Failure to respond to antibiotic treatment within 72

hours should prompt reconsideration of the diagnosis and empiric treatment regimen as
well as an assessment for complications. (See 'Clinical failure' above and 'Nonresolving
CAP' above.)
● Prevention − Key preventive measures include smoking cessation (when appropriate),

influenza vaccination for the general population, and pneumococcal vaccination for at-
risk populations. (See 'Prevention' above.)
ACKNOWLEDGMENT
We are saddened by the death of John G Bartlett, MD, who passed away in January 2021.
UpToDate gratefully acknowledges his tenure as the founding Editor-in-Chief for UpToDate in
Infectious Diseases and his dedicated and longstanding involvement with the UpToDate
program.
Use of UpToDate is subject to the Terms of Use.
Topic 117561 Version 27.0
GRAPHICS
Pneumonia terminology
Term Definition
Classification by site of acquisition
Community-acquired An acute infection of the pulmonary parenchyma acquired outside

pneumonia (CAP) of health care settings
Nosocomial pneumonia An acute infection of the pulmonary parenchyma acquired in

hospital settings, which encompasses hospital-acquired pneumonia
and ventilator-associated pneumonia
Hospital-acquired Pneumonia acquired ≥48 hours after hospital admission; includes

pneumonia (HAP) both HAP and VAP
Ventilator-associated Pneumonia acquired ≥48 hours after endotracheal intubation

pneumonia (VAP)
Health care-associated Retired term, which referred to pneumonia acquired in health care
pneumonia (HCAP) facilities (eg, nursing homes, hemodialysis centers) or after recent
hospitalization*
Classification by etiology
Atypical pneumonia Pneumonia caused by "atypical"¶ bacterial pathogens including

Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae,
Chlamydia psittaci, and Coxiella burnetii
Aspiration pneumonia Pneumonia resulting from entry of gastric or oropharyngeal fluid,

which may contain bacteria and/or be of low pH, or exogenous
substances (eg, ingested food particles or liquids, mineral oil, salt or
fresh water) into the lower airways
Chemical pneumonitis Aspiration of substances (eg, acidic gastric fluid) that cause an
inflammatory reaction in the lower airways, independent of
bacterial infection
Bacterial aspiration An active infection caused by inoculation of large amounts of

pneumonia bacteria into the lungs via orogastric contents
* The term HCAP was used to identify patients at risk for infection with multidrug-resistant
pathogens. This categorization may have been overly sensitive, leading to increased,
inappropriately broad antibiotic use.
¶ The origin of the term "atypical" is a matter of debate. The term may refer to the fact that these
organisms are not "typical" bacteria, which cannot be identified by standard microbiologic
techniques. Others suggest that atypical refers to the mild nature of the pneumonia caused by
some of these organisms compared with pneumonia caused by Streptococcus pneumoniae.
Graphic 130821 Version 3.0
The impact of age on the incidence of patients hospitalized with community-ac

pneumonia in the United States
Reproduced from: Ramirez JA, Wiemken TL, Peyrani P, et al. Adults hospitalized with pneumonia in the United States: Incidence,
epidemiology, and mortality. Clin Infect Dis 2017; 65(11):1806-1812. By permission of Oxford University Press on behalf of the Infec
Diseases Society of America. Copyright © 2017.
The impact of comorbid conditions on the incidence of patients hospitalized wi

community-acquired pneumonia in the United States
CHF: congestive heart failure; COPD: chronic obstructive pulmonary disease.
Reproduced from: Ramirez JA, Wiemken TL, Peyrani P, et al. Adults hospitalized with pneumonia in the United States: Incidence,
epidemiology, and mortality. Clin Infect Dis 2017; 65(11):1806-1812. By permission of Oxford University Press on behalf of the Infec
Diseases Society of America. Copyright © 2017.
Microbial etiology of community-acquired pneumonia by site of care*
Outpatients Ward patients Int

United
Spain[1] Canada[2] Spain[1]
States[3]
Total patients 514 507 2521 585 488

evaluated
Patients in 161 (31.3) 244 (48.1) 1042 (41) 120 (21) 260 (5
whom a
pathogen was
identified
Patients in 353 (68.7) 263 (51.9) 1479 (59) 465 (79) 228 (4
whom no
pathogen was
identified
Pathogen¶
Streptococcus 56 (10.9) 30 (5.9) 447 (17.7) 38 (6.5) 110 (2

pneumoniae
Other 0 5 (1.0) 0 0 0
Streptococcus
spp
Haemophilus 8 (1.6) 25 (4.9) 54 (2.1) 16 (2.7) 8 (1.6

influenzae
Haemophilus 0 10 (2.0) 0 0 0
parainfluenzae
Moraxella 0 6 (1.2) 4 (0.2) 0 1 (0.2

catarrhalis
Legionella 10 (1.9) Δ 87 (3.5) ◊ 21 (4.

pneumophila
Mycoplasma 27 (5.3)§ 87 (17.2)§ 32 (1.3)§ ¥ 6 (1.2

pneumoniae
Chlamydia 10 (1.9)§ 72 (14.2)§ 32 (1.3)§ ¥ 8 (1.6

pneumoniae
Coxiella 11 (2.1)§ Δ 17 (0.7)§ ¥ 2 (0.4

burnetii
Staphylococcus 1 (0.2) 6 (1.2) 18 (0.7) 25 (4.3) 6 (1.2

aureus
MSSA 1 (0.2) NR 9 (0.4) 18 (3.1) 4 (0.8

MRSA 0 NR 9 (0.4) 7 (1.2) 2 (0.4
Gram- 1 (0.2) 2 (0.4) 23 (0.9) 15 (2.6) 3 (0.6

negative
enteric bacilli
Pseudomonas 1 (0.2) 1 (0.2) 37 (1.5) 12 (2.1) 12 (2.

aeruginosa
Respiratory 15 (2.9)§ † 123 (4.9)§ † 10 (2.

viruses‡
Other 6 (1.2) 14 (2.8) 33 (1.3) 8 (1.4) 15 (3.

pathogen
>1 pathogen 15 (2.9) ** 135 (5.4) 6 (1.0) 58 (11
Diagnostic methods
Cultures (sputum, Cultures Cultures (sputum, Cultures Cultu

blood, transthoracic (sputum, blood, transthoracic (blood, blood
needle aspirate, blood), needle aspirate, endotracheal need
transbronchial serologic transbronchial aspirates, trans
aspirates, BAL fluid, testing (for aspirates, BAL fluid, protected aspir
protected specimen M. protected specimen specimen prote
brush respiratory pneumoniae, brush respiratory brush brush
samples, pleural C. samples, pleural respiratory samp
fluid), serologic pneumoniae) fluid), serologic samples, BAL fluid)
testing (for M. testing (for M. fluid, pleural testin
pneumoniae, C. pneumoniae, C. fluid), pneum
pneumoniae, L. pneumoniae, L. urinary pneum
pneumophila, C. pneumophila, C. antigen (for pneum
burnetti, influenza A burnetti, influenza A L. burne
and B, parainfluenza and B, parainfluenza pneumophila) and B
viruses 1 to 3, viruses 1 to 3, viruse
respiratory syncytial respiratory syncytial respi
virus, adenovirus), virus, adenovirus), virus,
urinary antigen urinary antigen urina
testing (for S. testing (for S. testin
pneumoniae and L. pneumoniae and L. pneum
pneumophila), pneumophila), pneum
immunofluorescence immunofluorescence immu
assay plus virus assay plus virus assay
isolation or reverse isolation or reverse isolat
transcriptase PCR for transcriptase PCR for trans
influenza A and B, influenza A and B, influe
parainfluenza parainfluenza parai
viruses 1 to 3, viruses 1 to 3, viruse
respiratory syncytial respiratory syncytial respi
virus, adenovirus virus, adenovirus virus,
MSSA: methicillin-susceptible Staphylococcus aureus; MRSA: methicillin-resistant Staphylococcus

aureus; NR: not reported; BAL: bronchoalveolar lavage; PCR: polymerase chain reaction.
* Results are reported as number of patients (percent). Different methods were used for
diagnosis in each study, as described in the row on diagnostic methods.
¶ Results are reported as the number of patients with a given pathogen, followed by the
percentage of patients in whom the pathogen was identified out of all of the patients in the
study. For example, in the first column, S. pneumoniae was detected in 30 of 507 patients in the
study (5.9%). Among the 244 patients in whom a pathogen was identified, S. pneumoniae was
detected in 12.3%.
Δ Testing for Legionella spp and C. burnetti was not performed.
◊ Legionella urinary antigen testing was performed in 35 ward patients and 26 intensive care unit
patients, but all results were negative. Legionella culture was not performed.
§ Pathogens detected by serologic methods may represent recent infection rather than active
infection.
¥ Testing for M. pneumoniae, C. pneumoniae, and C. burnetii was not performed.
‡ Influenza viruses A or B, parainfluenza viruses 1 to 3, respiratory syncytial virus, adenovirus.
† Testing for viruses was not performed.
** Some patients had >1 pathogen isolated, but the details were not reported.
References:
1. Cillóniz C, Ewig S, Polverino E, et al. Microbial aetiology of community-acquired pneumonia and its relation to
severity. Thorax 2011; 66:340.
2. Marrie TJ, Poulin-Costello M, Beecroft MD, Herman-Bnjidic Z. Etiology of community-acquired pneumonia treated in
an ambulatory setting. Resp Medicine 2005; 99:60.
3. Restrepo MI, Mortensen EM, Velez JA, et al. A comparative study of community-acquired pneumonia patients
admitted to the ward and the ICU. Chest 2008; 133:610.
Community-acquired pneumonia: Risk factors for specific pathogens in

adults
Condition Commonly encountered pathogen(s)
Alcohol use disorder Streptococcus pneumoniae, oral anaerobes, Klebsiella pneumoniae,

Acinetobacter species, Mycobacterium tuberculosis
COPD and/or smoking Haemophilus influenzae, Pseudomonas aeruginosa, Legionella species,

S. pneumoniae, Moraxella catarrhalis, Chlamydia pneumoniae
Aspiration Gram-negative enteric pathogens, oral anaerobes
Lung abscess CA-MRSA, oral anaerobes, endemic fungal pneumonia, M.

tuberculosis, atypical mycobacteria
Exposure to bat or bird Histoplasma capsulatum

droppings
Exposure to birds Chlamydia psittaci (if poultry: avian influenza)
Exposure to rabbits Francisella tularensis
Exposure to farm animals Coxiella burnetti (Q fever)

or parturient cats
HIV infection (early) S. pneumoniae, H. influenzae, M. tuberculosis
HIV infection (late) The pathogens listed for early infection plus Pneumocystis jirovecii,
Cryptococcus, Histoplasma, Aspergillus, atypical mycobacteria
(especially Mycobacterium kansasii), P. aeruginosa, H. influenzae
Hotel or cruise ship stay in Legionella species

previous two weeks
Travel to or residence in Coccidioides species, hantavirus

southwestern United States
Travel to or residence in Burkholderia pseudomallei, avian (H5N1, H7N9) influenza, SARS

Southeast and East Asia coronavirus
Travel to or residence in the Middle East respiratory syndrome coronavirus

Arabian peninsula
Influenza active in Influenza, S. pneumoniae, Staphylococcus aureus, H. influenzae

community
Cough >2 weeks with Bordetella pertussis

whoop or posttussive
vomiting
Structural lung disease (eg, P. aeruginosa, Burkholderia cepacia, S. aureus

bronchiectasis)
Injection drug use S. aureus, anaerobes, M. tuberculosis, S. pneumoniae
Endobronchial obstruction Anaerobes, S. pneumoniae, H. influenzae, S. aureus
In context of bioterrorism Bacillus anthracis (anthrax), Yersinia pestis (plague), Francisella

tularensis (tularemia)
The most commonly identified causes of community-acquired pneumonia include respiratory

viruses (particularly SARS coronavirus 2 during the pandemic), typical bacteria (eg, S. pneumoniae,
H. influenzae, M. catarrhalis), and atypical bacteria (eg, Legionella spp, Mycoplasma pneumoniae, C.
pneumoniae). The relative prevalence of these pathogens varies with geography, pneumococcal
vaccination rates, patient risk factors, season, and pneumonia severity. Certain epidemiologic
exposures, like those listed above, also raise the likelihood of infection with a particular
pathogen.
COPD: chronic obstructive pulmonary disease; CA-MRSA: community-acquired methicillin-

resistant Staphylococcus aureus; HIV: human immunodeficiency virus; SARS: severe acute
respiratory syndrome.
Adapted with permission from: Mandell, LA, Wunderink, RG, Anzueto, A, et al. Infectious Diseases Society of
America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults.
Clin Infect Dis 2007; 44:S27. Copyright © 2007 University of Chicago Press.
Risk factors for CAP caused by MRSA and Pseudomonas
MRSA Pseudomonas
Strong risk Known MRSA colonization Known Pseudomonas colonization

factors*
Prior MRSA infection Prior Pseudomonas infection
Detection of gram-positive cocci in Detection of gram-negative rods on a

clusters on a good-quality sputum good-quality sputum Gram stain
Gram stain
Hospitalization with receipt of IV
antibiotics in the prior 3 months
Other factors Recent hospitalization or antibiotic Recent hospitalization or stay in a

that should raise use, particularly hospitalization with long-term care facility
suspicion for receipt of IV antibiotics in the prior 3
infection¶ months
Recent influenza-like illness Recent antibiotic use of any kind
Necrotizing or cavitary pneumonia Frequent COPD exacerbations

requiring glucocorticoid and/or
antibiotic use
EmpyemaΔ Other structural lung diseases (eg,

bronchiectasis, cystic fibrosis)
Immunosuppression Immunosuppression
Risk factors for MRSA colonization,

including:
End-stage kidney disease
Crowded living conditions (eg,
incarceration)Δ
Injection drug useΔ
Contact sports participationΔ
Men who have sex with menΔ
CAP: community-acquired pneumonia; MRSA: methicillin-resistant Staphylococcus aureus; IV:

intravenous; COPD: chronic obstructive pulmonary disease.

* The presence of these risk factors generally warrant empiric treatment in patients with CAP of
any severity.

¶ The presence of these factors should raise suspicion for MRSA or Pseudomonas infection and
generally warrants treatment in those who are severely ill; in others, the need for empiric
treatment should take into account local prevalence, severity of illness, and overall clinical
assessment.

Δ This factor is associated with community-acquired MRSA infection, which can cause severe
toxin-mediated infection. Refer to the UpToDate topic on MRSA infections and treatment of CAP in
patients with risk factors for MRSA infection for further detail.
Community-acquired pneumonia (CAP) pathogenesis
Traditionally, CAP is thought to be caused by inhalation or aspiration of a respiratory

pathogen into an otherwise sterile alveoli. The local inflammatory response to the
pathogen results in pulmonary signs and symptoms such as cough, sputum
production, dyspnea, crackles, and hypoxemia. Release of cytokines into
the bloodstream leads to the systemic signs or symptoms of pneumonia, which often
include fever, fatigue, tachycardia, and leukocytosis.
With the discovery of the lung microbiome, the traditional model has evolved. When a
respiratory pathogen arrives in the alveolar space, it likely has to compete with
resident microbes to replicate. Additionally, resident microbes may also modulate the
host immune response to the infecting pathogen. Hypothetically, CAP might also arise
from uncontrolled replication of microbes that normally reside in the alveoli.
Pneumococcal pneumonia chest radiograph
64-year-old male with insulin-dependent diabetes mellitus. He was

admitted with bacteremic pneumococcal pneumonia. Note the left
lower lobe opacity.
Courtesy of Thomas J Marrie, MD.
Plain radiograph: Mycoplasma pneumoniae pneumonia
Diffuse bilateral interstitial infiltrates with M. pneumoniae infection.
Courtesy of Dwight A Powell, MD.
Pneumonia bulging fissure
Chest radiograph from a 55-year-old female with bacteremic

pneumococcal pneumonia. Shows a dense left lower lobe opacity
with a bulging fissure.
Courtesy of Thomas J Marrie, MD.
Chest radiograph of Pneumocystis jirovecii pneumonia with ground-glass opacif
Chest radiograph in patients with Pneumocystis jirovecii pneumonia, one that shows perihilar ground-glas
opacification with early consolidation (A) and the other that shows left-sided ground-glass opacification a
right-sided early consolidation (B).
Mycoplasma pneumonia
Chest radiograph (A) shows a bilateral reticulonodular pattern. High-resolution

computed tomography (CT) image at the level of the main bronchi (B) demonstrates
bilateral ground-glass opacities and centrilobular nodules (arrows). High-resolution
CT scan at the level of the basal segmental bronchi (C) shows centrilobular nodules
(straight arrows), branching opacities (tree-in-bud pattern; curved arrow), ground-
glass opacities, small foci of consolidation, and mild thickening of the interlobular
septa (arrowheads). The patient was a 20-year-old man with Mycoplasma pneumoniae
pneumonia.
Reproduced with permission from: Viruses, Mycoplasma, and Chlamydia. In: Imaging of Pulmonary
Infections, Müller NL, Franquet T, Lee KS (Eds), Lippincott Williams & Wilkins, Philadelphia 2007. Copyright ©
2007 Lippincott Williams & Wilkins. www.lww.com.
Complications of Streptococcus pneumoniae

pneumonia
Radiographic images of the complications of pneumococcal

pneumonia.
(Left panel) Lung abscess with an air-fluid level in the right lung.
Abscess cavity material is nearly always culture positive, and patients
commonly defervesce within 48 hours of interventional drainage.
(Right panel) Radiograph of necrotizing pneumonia in the left lung.
Community-acquired pneumonia: Determining the appropriate site of treatme
ICU: intensive care unit; ED: emergency department; PSI: Pneumonia Severity Index; PaO2: partial pressu
oxygen; CURB-65: confusion, uremia, respiratory rate, blood pressure, age ≥ 65 years; CAP: community-a
* Among the available scoring systems for determining the need for admission in patients with CAP, we p
studied and validated. If a less complex scoring system is desired, the CURB-65 score is a reasonable alte
safety in guiding the initial site of treatment have not been empirically assessed. Refer to the UpToDate t
determining the appropriate site of care in patients with CAP for additional details and to access PSI and
¶ Scoring systems, such as the PSI and CURB-65, and clinical criteria are intended to supplement rather
physician. Factors other than the predictors included in the rules and the clinical criteria may be importa
decision or selecting the site of inpatient care. As examples, patients with early signs of sepsis or rapidly
represented by severity scores. Patients with these features may warrant hospitalization and/or ICU adm
older age may be overrepresented in severity scores; this should be taken into account when determinin
Δ Using the CURB-65 score, if the patient has a score of 1 because he or she is ≥65 years of age and he o
hospital admission is not necessarily indicated.
◊ Although a definitive etiologic diagnosis is often not established until after the site of treatment decisi
epidemiologic evidence favoring pathogens associated with rapidly progressive forms of pneumonia (eg,
severe acute respiratory syndrome, Middle East respiratory syndrome, avian influenza [eg, H5N1, H7N9],
disease 2019) indicate a need to perform close clinical follow-up to monitor severity of illness particularly
at presentation and treated outside of the hospital setting.
§ Some PSI class II and III patients may benefit from in-home health care support, also termed "hospital-
intravenous fluids, intravenous antibiotics).
Community-acquired pneumonia: Initial evaluation and site of care based

on severity assessment in adults
Microbiologic
Severity score* Site of care
evaluation
Mild PSI: I or II Ambulatory care COVID-19 testing

during the pandemic
or
Influenza testing
CURB-65: 0¶
(when incidence is
high and results
would change
management)Δ
Otherwise, testing is
usually not needed
Moderate PSI: III or IV General medical ward Blood cultures
or Sputum Gram stain

and culture
CURB-65: 1¶ to 2
Urine streptococcal
antigen
Legionella testing◊
Respiratory viral
panel during
respiratory virus
season§
COVID-19 testing¥
HIV screening‡
Severe PSI: IV or V ICU Blood cultures

or Sputum Gram stain
and culture
CURB-65: ≥3
Urine streptococcal
and/or antigen test
Fulfillment of ATS/IDSA Legionella testing◊
criteria for ICU Respiratory viral
admission† panel§
Bronchoscopy
specimens for Gram
stain, fungal stain,
aerobic, fungal
culture, and
molecular testing
(when feasible)**
COVID-19 testing¥
HIV screening‡
CAP presents along a continuum of severity. For practical purposes, we typically categorize CAP as
mild, moderate, or severe. Severity assessment is based on clinical judgement and can be aided
by severity scores, such as the PSI or the CURB-65 score. We generally prefer the PSI as it is better
validated; however, many clinicians prefer the CURB-65 as it is easier to use. The three levels of
severity correspond to the three levels of care (ambulatory care, hospital admission to the general
medical ward, and ICU). The severity assessment and site of care each inform the initial
microbiologic evaluation and empiric antibiotic selection. For all patients, we modify our
approach based on patient-specific factors such as epidemiologic exposures and ability to care
for oneself at home. Refer to the UpToDate topic on the treatment of CAP for further detail.
PSI: Pneumonia Severity Index; COVID-19: coronavirus disease 2019; ATS: American Thoracic
Society; IDSA: Infectious Diseases Society of America; ICU: intensive care unit; CAP: community-
acquired pneumonia; PCR: polymerase chain reaction; PaO2/FiO2: arterial oxygen tension to
fraction of inspired oxygen.
* Severity scores should be used as an adjunct to clinical judgment. Patients with early signs of
sepsis (eg, patients fulfilling minor ATS/IDSA criteria) or rapidly progressive illness are not well
represented in severity scoring systems. Patients with these features may warrant hospitalization
and/or ICU admission regardless of score. Conversely, older age may be overrepresented in
severity scores; this should be taken into account when determining site of care.
¶ Because age >65 years is a criterion in the CURB-65 score, patients with CURB-65 scores of 1
who are older than 65 years may also be reasonably treated in the ambulatory setting.
Δ Refer to the UpToDate content on the diagnosis of influenza for detail.
◊ PCR on sputum sample is preferred for the diagnosis of Legionella spp because it detects most
clinically relevant Legionella spp. The urine antigen test is an acceptable alternative when PCR is
not available but is specific for Legionella pneumophila serogroup 1.
§ The approach to testing for respiratory viruses varies among institutions. At a minimum, testing
for influenza by PCR should be performed. However, testing is often expanded to include
adenovirus, parainfluenza, respiratory syncytial virus, and human metapneumovirus. The
specific assay used (eg, PCR, serology, culture) may also vary among institutions. Results from
multiplex PCR assays should be interpreted with caution because most multiplex PCR assays have
not been approved for use on lower respiratory tract specimens.
¥ Testing for COVID-19 is recommended for all patients during the pandemic. Refer to the related
UpToDate content on the approach to testing.
‡ Refer to UpToDate content on screening and diagnosis of HIV infection for detail.
† ATS and IDSA major criteria for ICU admission include either septic shock with need for
vasopressor support and/or respiratory failure with need for mechanical ventilation. If major
criteria are not met, patients should also be considered for ICU admission if 3 or more of the
following minor criteria are present: altered mental status, hypotension requiring fluid support,
temperature <36°C/96.8°F, respiratory rate ≥30 breaths/minute, PaO2/FiO2 ratio ≤250, blood
urea nitrogen ≥20 mg/dL (7 mmol/L), leukocyte count <4000 cells/microL, platelet count
<100,000/mL, or multilobar infiltrates.
** We generally weigh the benefits of obtaining a microbiologic diagnosis against the risks of the
bronchoscopy (eg, need for intubation, bleeding, bronchospasm, pneumothorax) on a case-by-
case basis. When pursuing bronchoscopy, we usually send specimens for aerobic and anaerobic
culture, Legionella culture, fungal stain and culture, and testing for viral pathogens (influenza,
adenovirus, parainfluenza, respiratory syncytial virus, and human metapneumovirus).
Distinguishing acute bronchitis from pneumonia in adults
Community-acquired pneumonia: Empiric outpatient antibiotic selection in adu
For all patients, our empiric regimens are designed to target:◊

Streptococcus pneumoniae (most common bacterial CAP pathogen)
Atypical pathogens (eg, Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae)

Coverage is expanded in those with comorbidities, older age, or recent antibiotic use to include or better
Beta-lactamase-producing Haemophilus influenzae
Moraxella catarrhalis
Methicillin-susceptible Staphylococcus aureus
For patients with structural lung disease (eg, advanced COPD), coverage is further expanded to include E
Escherichia coli and Klebsiella spp.
ATS/IDSA: American Thoracic Society/Infectious Diseases Society of America; COPD: chronic obstructive p
community-acquired pneumonia; IgE: immunoglobulin E.
* Major comorbidities include but are not limited to chronic heart, renal, or liver disease, diabetes mellit
immunosuppression.
¶ Patients with mild non-IgE-mediated reactions (eg, maculopapular rash) to penicillin or known cephalo
use later-generation cephalosporins safely. Patients with IgE-mediated reactions (hives, angioedema, ana
reactions should generally use other agents. Refer to the UpToDate text on penicillin hypersensitivity rea
Δ Reasons to avoid macrolides include baseline prolonged QTc interval or risk for QTc prolongation (eg, h
clinically significant bradycardia, or use of other QT-prolonging agents).
◊ Our approach differs from the ATS/IDSA, which recommend monotherapy with amoxicillin, doxycycline
macrolide resistance is low) as options for patients without comorbidities or risk factors for drug-resistan
prefer to treat all patients with a regimen that treats most strains of drug-resistant S. pneumoniae and aty
patients because the potential to reduce morbidity is high and the downside of a short course of therapy
to the UpToDate text for detail.
§ For macrolides, resistance rates among S. pneumoniae are often >30% in the United States and typically
world, apart from some regions in Northern Europe. For doxycycline, resistance rates are less well establ
to 20% in the United States and likely rising.
¥ Lefamulin is a newer agent that is active against most CAP pathogens including S. pneumoniae, H. influe
and atypical pathogens. Although lefamulin lacks activity against Enterobacteriaceae (eg, Klebsiella spp a
appropriate for patients with structural lung disease, its more targeted spectrum makes it less disruptive
experience with lefamulin is limited, and it is not recommended in moderate to severe hepatic dysfunctio
known long QT syndrome, or with concomitant QT-prolonging agents. There are drug interactions with C
substrates; in addition, lefamulin tablets are contraindicated with QT-prolonging CYP3A4 substrates. Ref
monograph and UpToDate text for detail.
‡ Omadacycline is another newer agent that is active against most CAP pathogens, including Enterobacte
alternative for patients who cannot tolerate beta-lactams (or other agents) and want to avoid fluoroquino
Groups at high risk for influenza complications
Children <5 years, but especially <2 years*
Adults ≥65 years of age
People who are pregnant or up to 2 weeks postpartum
Residents of nursing homes and long-term care facilities
Non-Hispanic Black persons, Hispanic or Latino persons, and American Indian or Alaska Native
persons¶
People with medical conditions including:

Asthma
Neurologic and neurodevelopmental conditions (including disorders of the brain, spinal
cord, and peripheral nerve and muscle such as cerebral palsy, epilepsy, stroke, intellectual
disability, moderate-to-severe developmental delay, muscular dystrophy, and spinal cord
injury)
Chronic lung disease (eg, chronic obstructive pulmonary disease, cystic fibrosis)
Heart disease (eg, congenital heart disease, congestive heart failure, coronary artery
disease)
Blood disorders (eg, sickle cell disease)
Endocrine disorders (eg, diabetes mellitus)
Kidney disorders
Liver disorders
Metabolic disorders (eg, inherited metabolic disorders and mitochondrial disorders)
Weakened immune system due to disease (eg, HIV, AIDS, cancer) or medication (eg,
chemotherapy or radiation therapy, chronic glucocorticoids)
Children <19 years of age who are receiving long-term aspirin therapy
People with Class III obesity (body mass index [BMI] ≥40 or ≥140% of the 95th percentile
value)
* In young children, rates of hospitalization and mortality are greatest among those <6 months of
age.
¶ Possibly related to economic and social conditions (eg, poverty, multigenerational households,
limited access or barriers to influenza vaccination).
Adapted from: Centers for Disease Control and Prevention. Influenza: Who is at higher risk of flu complications. Available
at: https://www.cdc.gov/flu/highrisk/index.htm (Accessed on February 11, 2022).
Community-acquired pneumonia: Empiric antibiotic selection for adults admitt
CAP: community-acquired pneumonia; MRSA: methicillin-resistant Staphylococcus aureus; PCR: polymerase
* This algorithm is intended for patients in whom admission to a general medical ward is considered app
should be administered as soon as possible after diagnosing CAP. If the etiology of CAP has been identifi
epidemiologic evidence of coinfection, treatment regimens should be simplified and directed to that pat
¶ Individuals with a past reaction to penicillin that was mild (not Stevens Johnson syndrome, toxic epider
and did not have features of an immunoglobulin (Ig)E-mediated reaction can receive a broad-spectrum (t
Δ Empiric therapy with aztreonam plus levofloxacin plus an aminoglycoside is generally appropriate for p
preclude the use of penicillins, cephalosporins, and carbapenems. However, patients with a prior life-thr
unless evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can r
interim.
◊ Combination therapy with a beta-lactam plus a macrolide and monotherapy with a respiratory fluoroqu
observational studies have suggested that beta-lactam plus macrolide combination regimens are associa
immunomodulatory effects of macrolides. Furthermore, the severity of adverse effects (including the risk
resistance in colonizing organisms are generally thought to be greater with fluoroquinolones than with t
combination therapy with a beta-lactam plus a macrolide rather than monotherapy with a fluoroquinolon
C. difficile infection. Recent antibiotic use should also inform the decision about the most appropriate reg
fluoroquinolone should be chosen if possible, and vice versa.
§ Omadacycline and lefamulin are newer agents and potential alternatives for patients who cannot tolera
may be limited by availability and/or insurance coverage.
¥ Examples of contraindications include increased risk for a prolonged QT interval and allergy.
‡ Doxycycline should not be used in pregnant women.
† The combination of vancomycin and piperacillin-tazobactam has been associated with acute kidney inju
antipseudomonal/antipneumococcal beta-lactam, options include using a beta-lactam other than piperac
using linezolid instead of vancomycin.
** Ceftaroline has activity against MRSA but not Pseudomonas; because of its extended spectrum, it is of
Community-acquired pneumonia: Empiric antibiotic selection for adults admitt
CAP: community-acquired pneumonia; MRSA: methicillin-resistant Staphylococcus aureus; PCR: polymerase

* This algorithm is intended for patients in whom admission to an intensive care unit is considered appr
should be administered as soon as possible after diagnosing CAP. If the etiology of CAP has been identifi
epidemiologic evidence of coinfection, treatment regimens should be simplified and directed to that pat
¶ Individuals with a past reaction to penicillin that was mild (not Stevens Johnson syndrome, toxic epider
and did not have features of an immunoglobulin (Ig)E-mediated reaction can receive a broad-spectrum (t
Δ Empiric therapy with aztreonam plus levofloxacin plus an aminoglycoside is generally appropriate for p
preclude the use of penicillins, cephalosporins, and carbapenems. However, patients with a prior life-thr
unless evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can r
interim.
◊ Regimens containing either a macrolide or fluoroquinolone have been generally comparable in clinica
containing regimens are associated with better clinical outcomes for patients with severe CAP, possibly d
adverse effects (including the risk for Clostridioides [formerly Clostridium] difficile infection) and the risk of
with fluoroquinolones than with other antibiotic classes. For this reason, we generally favor a macrolide-c
macrolides, such as patient allergy or intolerance. Recent antibiotic use should also inform the decision a
prior three months, a fluoroquinolone should be chosen if possible, and vice versa.
§ The combination of vancomycin and piperacillin-tazobactam has been associated with acute kidney inju
antipseudomonal/antipneumococcal beta-lactam, options include using a beta-lactam other than piperac
favored, using linezolid instead of vancomycin.
¥ Ceftaroline has activity against MRSA but not Pseudomonas; because of its extended spectrum, it is ofte
Approach to the patient with a past penicillin reaction who requires antibiotics
This algorithm is intended for use in conjunction with the UpToDate content on choice of antibiotics in pe
patients but also applies to outpatients if test dose procedures can be performed in an appropriately mo
reactions, including anaphylaxis.
IgE: immunoglobulin E.
* Ask the following:

1. What exactly were the symptoms?
Raised, red, itchy spots with each lesion lasting less than 24 hours (hives/urticaria)?
Swelling of the mouth, eyes, lips, or tongue (angioedema)?
Blisters or ulcers involving the lips, mouth, eyes, urethra, vagina, or peeling skin (seen in SJS
Respiratory or hemodynamic changes (anaphylaxis)?
Joint pains (seen in serum sickness)?
Did the reaction involve organs like the kidneys, lungs, or liver (seen in DRESS, other severe
2. What was the timing of the reaction after taking penicillin: Minutes, hours, or days later? Was it aft
3. How long ago did the reaction happen? (After 10 years of avoidance, only 20% of patients with IgE-
4. How was the reaction treated? Was there a need for urgent care or was adrenaline/epinephrine ad
5. Has the patient tolerated similar medications, such as ampicillin, amoxicillin, or cephalexin since th
¶ Isolated mild hives, without other symptoms of an IgE-mediated reaction, can often occur in the setting
childhood or >10 years ago, may also be considered to be at minimal risk for a recurrent serious reaction
Δ This algorithm is intended for use in conjunction with additional UpToDate content. For a description of
topic on choice of antibiotics in penicillin-allergic hospitalized patients.
◊ Consult allergist to perform skin testing. If skin testing is not possible, patient may still be able to rece
desensitization (also known as tolerance induction) procedure. Refer to the UpToDate topic on rapid drug
Original figure modified for this publication. Blumenthal KG, Shenoy ES, Varughese CA, et al. Impact of a clinical guideline for prescri
Immunol 2015; 115:294. Illustration used with the permission of Elsevier Inc. All rights reserved.
Usual duration of findings in treated community-acquired pneumonia
Abnormality Duration (days)
Tachycardia and hypotension 2
Fever, tachypnea, and hypoxia 3
Cough 14
Fatigue 14
Infiltrates on chest radiograph 30
References:
1. Marrie TJ, Beecroft MD, Herman-Gnjidic Z. Resolution of symptoms in patients with community-acquired pneumonia
treated on an ambulatory basis. J Infect 2004; 49:302.
2. Metlay JP, Atlas SJ, Borowsky LH, Singer DE. Time course of symptom resolution in patients with community-acquired
pneumonia. Respir Med 1998; 92:1137.
3. Fine MJ, Stone RA, Singer DE, et al. Processes and outcomes of care for patients with community-acquired
pneumonia: results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study. Arch Intern Med
1999; 159:970.
Transitioning inpatients with community-acquired pneumonia from IV to

oral antibiotics
IV: intravenous.
* Patients should show some clinical response before switching to oral medications. Fever
may persist with lobar pneumonia. Cough from pneumococcal pneumonia may not clear for a
week; abnormal chest radiograph findings usually clear within 4 weeks but may persist for 12
weeks in older individuals and those with underlying pulmonary disease.
¶ Generally avoid in patients with known QT interval prolongation or risk factors for QT
interval prolongation.
Δ Dose adjustment is necessary in patients with renal insufficiency.
◊ Cefpodoxime has similar coverage to ceftriaxone and cefotaxime and is generally preferred
for patients with structural lung disease and others at risk for infection with
Enterobacteriaceae (eg, Escherichia coli, Klebsiella spp).
§ If the patient has already received 1.5 g of azithromycin, atypical coverage can be
discontinued.
Algorithm for procalcitonin-guided antibiotic discontinuation in clinically stable

patients with known or suspected community-acquired pneumonia*
CAP: community-acquired pneumonia.
* Procalcitonin has not been well studied in immunocompromised patients, trauma or surgery patients,
women, patients with cystic fibrosis, and patients with chronic kidney disease. The algorithm may not be
to these populations or other patients with complex comorbidities.
¶ Optimal thresholds have not been precisely determined. Some experts use a lower threshold, typically
when deciding to discontinue antibiotics.
Δ Decisions to stop antibiotics should be made in combination with clinical judgment and presume that t
stable and that a bacterial infection that requires a longer course of therapy, such as CAP complicated by
was not identified.
◊ Systemic inflammation due to other causes, such as burns, trauma, surgery, pancreatitis, malaria, or in
candidiasis can also lead to elevated procalcitonin levels.
§ Reaching a procalcitonin level of <0.25 ng/mL is not a requirement for antibiotic discontinuation. For pa
clinically resolved pneumonia and levels >0.25 ng/mL, clinical judgment alone is adequate.
Follow-up imaging for immunocompetent adults

who have recovered from community-acquired
pneumonia
Follow-up imaging is not needed for most patients who have

promptly recovered from CAP (eg, within 5 to 7 days for an
otherwise healthy person). However, follow-up clinic visits are
good opportunities to review the patient's risk for lung cancer
based on age, smoking history, and recent imaging findings.
CT: computed tomography; CAP: community-acquired pneumonia.
* Criteria for lung cancer screening vary among clinical practice

guidelines (eg, thresholds for age and duration of smoking
therapy). Refer to UpToDate text for detail.
¶ Exceptions include patients who are followed radiographically

for other reasons (eg, selected patients with advanced structural
lung disease). Whether patients with small pleural effusions
require follow-up is an open question. We generally do not obtain
follow-up imagining unless the patient is slow to recover or
develops new system or respiratory symptoms.

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7/9/22, 11:13 Overview of community-acquired pneumonia in adults - UpToDate

Official reprint from UpToDate®

Overview of community-acquired pneumonia in adults

Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality

Pneumonia is frequently categorized based on site of acquisition ( table 1).

● Community-acquired pneumonia (CAP) refers to an acute infection of the pulmonary

● Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma

• HAP refers to pneumonia acquired ≥48 hours after hospital admission.

• VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.

Health care-associated pneumonia (HCAP; no longer used) referred to pneumonia acquired in

● Impaired airway protection – Conditions that increase risk of macroaspiration of

Common causes — Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the

• S. pneumoniae (most common bacterial cause)

• Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or

• Influenza A and B viruses

● Decline in S. pneumoniae incidence – Although S. pneumoniae (pneumococcus) is the

Because pneumococcal vaccination rates vary regionally, the prevalence of S. pneumoniae

● The coronavirus disease 2019 (COVID-19) pandemic – SARS-CoV-2 is an important cause

● Increased recognition of other respiratory viruses – Respiratory viruses have been

Antimicrobial resistance — Knowledge of antimicrobial resistance patterns and risk factors

● Methicillin-resistant S. aureus (MRSA) is an uncommon cause of CAP. Risk factors for

In contrast with health care-associated MRSA, community-acquired MRSA (CA-MRSA)

The pathogenesis of CAP is discussed in greater detail separately. (See "Epidemiology,

● Pulmonary signs and symptoms – Cough (with or without sputum production),

Making the diagnosis — The diagnosis of CAP generally requires the demonstration of an

• Respiratory failure requiring mechanical ventilation

The presence of three of these criteria warrants ICU admission:

• Altered mental status

• Blood urea nitrogen (BUN) ≥20 mg/dL (7 mmol/L)

Microbiologic testing — The benefit of obtaining a microbiologic diagnosis should be

respiratory viruses (eg, influenza, adenovirus, parainfluenza, respiratory syncytial virus,

● For immunocompromised patients, we broaden our differential to include opportunistic

viral pathogens such as cytomegalovirus. The approach to diagnostic testing varies

• Congestive heart failure with pulmonary edema

• Acute exacerbation of bronchiectasis

Respiratory illnesses that mimic CAP or co-occur with CAP include:

• Acute exacerbations of chronic obstructive pulmonary disease

The management of COVID-19 is discussed in detail elsewhere. (See "COVID-19: Management

Alternatives to amoxicillin-based regimens include combination therapy with a cephalosporin

In the absence of hepatic impairment or drug interactions, lefamulin is a potential

Inpatient antibiotic therapy

hospitalized patient with known or suspected influenza. (See "Seasonal influenza in

For patients with penicillin hypersensitivity reactions, we select an appropriate agent

Adjunctive glucocorticoids — The use of glucocorticoids as an adjunctive treatment for

Disposition — Once a patient with CAP is hospitalized, further management will be dictated

Antibiotic de-escalation — For patients in whom a causative pathogen has been

Duration of therapy — We generally determine the duration of therapy based on the

Discharge — Hospital discharge is appropriate when the patient is clinically stable, can

Immunocompromised patients — The spectrum of potential pathogens expands

Because management is complex, drug interactions are common, adjustments in

COMPLICATIONS AND PROGNOSIS

Clinical failure — Clear indicators of clinical failure include progression to sepsis and/or

Reasons for clinical failure generally fall into these categories:

Other possibilities include infection with a drug-resistant pathogen or an unusual

● Development of comorbid complications – Comorbid complications may be infectious

● Loculated infection – Patients with complications such as lung abscess, empyema, or

● Bronchial obstruction – Bronchial obstruction (eg, by a tumor) can cause a

● Pathogens that cause subacute/chronic CAP – Mycobacterium tuberculosis,

Once a patient is characterized as having nonresolving CAP, a complete new physical

● Smoking cessation (when appropriate)