Community-Acquired Pneumonia (CAP)

Updated: Jul 25, 2016

Author: Stephanie L Baer, MD; Chief Editor: Michael Stuart Bronze, MD more...

OVERVIEW

Practice Essentials
Community-acquired pneumonia (CAP) is one of the most common infectious diseases and is an important
cause of mortality and morbidity worldwide. Typical bacterial pathogens that cause CAP include
Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis (see images below).
However, with the advent of novel diagnostic technologies, viral respiratory tract infections are being
identified as common etiologies of CAP. The most common viral pathogens recovered from hospitalized
patients admitted with CAP include human rhinovirus and influenza. [1]

Gram stain showing Streptococcus pneumoniae.

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Gram stain showing Haemophilus influenzae.

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Presentation and pathogens in typical community-acquired pneumonia

The term typical CAP refers to a bacterial pneumonia caused by pathogens such as S pneumoniae, H
influenzae, and M catarrhalis. Patients with typical CAP classically present with fever, a productive cough
with purulent sputum, dyspnea, and pleuritic chest pain. Characteristic pulmonary findings on physical
examination include the following:

Tachypnea
Rales heard over the involved lobe or segment
Increased tactile fremitus, bronchial breath sounds, and egophony may be present if consolidation
has occurred.
Decreased tactile fremitus and dullness on chest percussion may result from parapneumonic effusion
or empyema.

Epidemiologic data may provide clues to the specific pathogen causing CAP, as follows:

The most common overall pathogen is S pneumoniae

Underlying chronic obstructive pulmonary disease (COPD) [2] : H influenzae or M catarrhalis
Recent influenza infection [3] : Staphylococcus aureus
Alcoholic patient presenting with currant jelly sputum : Klebsiella pneumoniae [2]

Atypical community-acquired pneumonia

The clinical presentation of so-called atypical CAP is often subacute and frequently indolent. In addition,
patients with atypical CAP may present with more subtle pulmonary findings, nonlobar infiltrates on
radiography, and various extrapulmonary manifestations (eg, diarrhea, otalgia). Atypical CAP pathogens
include the following:

Mycoplasma pneumoniae
Chlamydophila ( Chlamydia) pneumoniae
Legionnaires disease ( Legionella pneumophila)
Respiratory viruses, including the following:
Influenza A and B
Rhinovirus
Respiratory syncytial virus
Human metapneumovirus
Adenovirus 4 and 7
Parainfluenza virus
Other rare viral pneumonias include the following:
Coxsackievirus
Echovirus
Coronavirus (MERS-CoV, SARS)
Hantavirus
Epstein-Barr virus
Cytomegalovirus
Herpes simplex virus
Human herpesvirus 6
Varicella-zoster virus
Psittacosis ( Chlamydophila psittaci)
Q fever ( Coxiella burnetii)
Tularemia ( Francisella tularensis)Endemic fungi (causing subacute or chronic pneumonia), as
follows:
Histoplasma capsulatum
Cryptococcus neoformans neoformans and neoformans gattii
 Coccidioides immitis
Mycobacteria: Mycobacteria tuberculosis and nontuberculous mycobacteria (uncommon)

Extrapulmonary signs and symptoms seen in some forms of atypical CAP may include the following:

Mental confusion
Prominent headaches
Myalgias
Ear pain
Abdominal pain
Diarrhea
Rash (Horder spots in psittacosis; erythema multiforme in Mycoplasma pneumonia)
Nonexudative pharyngitis
Hemoptysis
Splenomegaly
Relative bradycardia

While historical clues and physical examination findings may suggest a causative pathogen, the clinical
signs and symptoms of CAP are not sufficiently specific to reliably differentiate the exact etiologic agent. [4]
Therefore, additional testing remains necessary to identify the pathogen and to optimize therapy in CAP.

Workup
Standard diagnostic studies for CAP include the following:

Chest radiography
Sputum Gram stain and/or culture
Blood cultures

Other laboratory tests

Depending on the perceived severity of illness and suspected etiology, additional workup may be
warranted, including the following:

Complete blood cell (CBC) count with differential

Serum sodium level
Serum blood urea nitrogen (BUN) and creatinine levels
Serum transaminase levels
Serum phosphorus level
Lactic acid level
Creatine phosphokinase (CPK)
C-reactive protein (CRP)
Lactate dehydrogenase (LDH)
Procalcitonin
Cold agglutinin titers
Urinary antigen testing for Legionella species and S pneumoniae
Serologic studies for M pneumoniae, C pneumoniae, Bordetella pertussis, C burnetii
Molecular diagnostics, ie, polymerase chain reaction (PCR) testing

Chest radiography

Obtain chest radiographs in all patients with suspected CAP to evaluate for an infiltrate compatible with the
presentation of CAP and to help exclude conditions that may mimic CAP (ie, lung cancer, pulmonary
emboli). [5, 6] Patients who present very early with CAP may have negative findings on chest radiography. In
these patients, repeat chest radiography within 24 hours may be beneficial. CT scanning may also be
necessary in immunocompromised patients who present with symptoms that suggest CAP in whom chest
radiography findings are negative. Serial chest radiography can be used to observe the progression of
CAP; however, radiographic improvement may lag behind clinical improvement.

Hospital admission
Multiple scoring systems are available to assess the severity of CAP and to assist in deciding whether a
patient should be hospitalized or admitted to the intensive care unit (ICU). The CURB-65 (confusion,
uremia, respiratory rate, low blood pressure, age >65 years) and the Pneumonia Severity Index (PSI) are
currently recommended by the 2007 Infectious Diseases Society of America/American Thoracic Society
Consensus Guidelines. [7] Patients with CURB-65 scores of 2 or more or PSI class IV-V may necessitate
hospitalization or more intensive in-home services. ICU is recommended for any patient who requires
mechanical ventilation or vasopressors. ICU admission should also be considered in patients with 3 or more
minor risk factors, including respiratory rate of 30 or more, PaO2/FiO2<250, multilobar infiltrates, confusion,
uremia, leukopenia, thrombocytopenia, hypothermia, and hypotension requiring aggressive fluid
resuscitation.

Proposed scoring systems may also be helpful in certain populations to predict the severity of CAP. The
SMART-COP score emphasizes the ability to predict the need for ventilator or vasopressor support and
includes systolic blood pressure, multilobar infiltrates, serum albumin levels, respiratory rate, tachycardia,
confusion, oxygenation, and pH level. The A-DROP (age, dehydration, respiratory failure, orientation,
systolic blood pressure) is also a severity score. Recently, an expanded CURB-65 has been shown to
improve prediction of 30-day mortality. It includes LDH, thrombocytopenia, and serum albumin, along with
the traditional CURB-65, and has been shown to have better prediction accuracy. [8]

Antibiotic Therapy

Adequate antimicrobial therapy for CAP includes coverage for S pneumoniae and atypical bacterial
pathogens. Outpatient treatment for CAP in patients with no comorbidities and no risk factors for drug-
resistant S pneumoniae frequently includes the following: [7]

A macrolide (azithromycin, clarithromycin, or erythromycin)

Doxycycline

Treatment in patients with comorbidities such as chronic heart, lung, liver, or renal disease; diabetes
mellitus; alcoholism; malignancy; asplenia; immunosuppression; prior antibiotics within 90 days; or other
risk factors for drug-resistant infection includes the following:

Respiratory fluoroquinolones (moxifloxacin, levofloxacin)

Beta-lactam (high-dose amoxicillin 1 g 3 times/day) or amoxicillin/clavulanate (2 g twice daily), or
ceftriaxone, cefpodoxime, or cefuroxime (500 mg twice daily) plus a macrolide or doxycycline

In regions with high rates of macrolide-resistant S pneumoniae, consider a nonmacrolide alternative.

For hospitalized patients, therapy consists of the following:

Beta-lactams (ceftriaxone or cefotaxime) plus a macrolide or

Respiratory fluoroquinolone

Recent studies have suggested that a beta-lactam alone may be noninferior to a beta-lactam/macrolide
combination or fluoroquinolone therapy in hospitalized patients. [9]

Therapy in ICU patients includes the following:

 Beta-lactam (ceftriaxone, cefotaxime, or ampicillin/sulbactam) plus either a macrolide or respiratory
fluoroquinolone
For patients with penicillin allergy, a respiratory fluoroquinolone and aztreonam

If Pseudomonas is suspected, therapy is as follows:

Anti-pneumococcal and anti-pseudomonal beta-lactam (piperacillin/tazobactam, cefepime,

carbapenem [imipenem, meropenem, or doripenem]) plus ciprofloxacin or levofloxacin or
Beta-lactam (as above) plus aminoglycoside and azithromycin or aminoglycoside and fluoroquinolone
For patients with penicillin allergy, aztreonam instead of the beta-lactam in the regimen listed above

If methicillin-resistant S aureus (MRSA) is suspected, vancomycin, linezolid, or ceftaroline should be added.

Rapid initiation of therapy is important for improved outcomes in CAP, although blanket measures to hasten
treatment are not without potential negative consequences. Quality-improvement efforts aimed at the
administration of antibiotics within a certain time period have contributed to increased inappropriate
antibiotic use and increased incidence of Clostridium difficile colitis. Nevertheless, in patients with signs of
severe CAP or sepsis, antibiotics should be given within the first hour of hypotension onset to reduce
mortality. [10] Cultures of respiratory specimens, blood, and pleural fluid; PCR of respiratory samples; or
antigen tests should be used to target therapy whenever possible. Inpatient CAP therapy usually consists of
intravenous antibiotics followed by transition to an oral course of therapy. [11, 12, 13, 14] Patients who are
severely ill or who are unable to tolerate or absorb oral medications may require a longer duration of
parenteral therapy before switching to an oral antibiotic. [15]

Mild to moderately ill patients with CAP may be treated entirely via the oral route, on either an inpatient or
outpatient basis. The duration of therapy for uncomplicated CAP is usually 5-7 days. [7, 10] Patients should
be afebrile for 48-72 hours and have no signs of instability before antibiotic therapy is stopped. The duration
of therapy may need to be increased if the initial empiric therapy has no activity against the specific
pathogen.

Immunocompromised hosts who present with CAP are treated in the same manner as otherwise healthy
hosts but may require a longer duration of therapy. Investigations into pathogens associated with
compromised hosts may need to be pursued.

Overview
Community-acquired pneumonia (CAP) is one of the most common infectious diseases addressed by
clinicians and is an important cause of mortality and morbidity worldwide.

Numerous pathogens can cause CAP. Typical bacterial pathogens that cause CAP include S pneumoniae,
H influenzae, and M catarrhalis. Numerous other organisms can cause CAP in the appropriate clinical
setting. Furthermore, the so-called atypical CAP pathogens are actually common causes of CAP and were
originally classified as atypical because they are not readily detectable on Gram stain or cultivatable on
standard bacteriologic media.

CAP is usually acquired via inhalation or aspiration of a pathogenic organism.

Aspiration pneumonia is commonly caused by various pathogens (eg, aerobic/anaerobic oral organisms).

Severe community-acquired pneumonia

Severe CAP frequently develops in individuals with comorbid factors such as underlying cardiopulmonary
disease, diminished splenic function, and/or heightened pathogenic virulence. Even in young and/or healthy
hosts, severe CAP can develop if the causative pathogen is sufficiently virulent. For example, influenza,
severe acute respiratory syndrome (SARS), Hantavirus pulmonary syndrome (HPS), and Legionnaires
disease may present as severe CAP. [16, 17, 18, 19]

Patients with severe CAP should have the benefit of an infectious disease specialist to assist in the
underlying cause of their condition.

Complications associated with community-acquired pneumonia

Complications in CAP depend on the infecting pathogen and the patients baseline health. For example,
various organisms can cause empyema, including S pneumoniae, K pneumoniae (classically occurring in
patients with chronic alcoholism), group A Streptococcus, and S aureus. Cavitation is not a typical feature of
pneumococcal pneumonia but is relatively common in K pneumoniae infections.

On occasion, myocardial infarction can be precipitated by community-acquired pneumonia (CAP).

Patients with CAP who have impaired splenic function may develop overwhelming pneumococcal sepsis,
potentially leading to death within 12-24 hours, regardless of the antimicrobial regimen used.

Morbidity and mortality

Morbidity and mortality associated with CAP are most common in elderly patients and immunocompromised
hosts.

Other factors that can predispose to morbidity and mortality in individuals with CAP include significant
comorbidities such as an increased respiratory rate, hypotension, fever, multilobar involvement, anemia,
and hypoxia. [20]

For more information, see the following:

Mycoplasma Pneumonia
Bacterial Pneumonia
Viral Pneumonia
Imaging Pneumocystis Carinii Pneumonia
Aspiration Pneumonia
Nosocomial Pneumonia
Ventilator-Associated Pneumonia
Pneumocystis (carinii) jiroveci Pneumonia
Fungal Pneumonia
Immunocompromised Pneumonia
Nursing Home Acquired Pneumonia
Chlamydial Pneumonia
Lymphocytic Interstitial Pneumonia
Imaging Typical Bacterial Pneumonia
Imaging Atypical Bacterial Pneumonia
Imaging Viral Pneumonia

Etiology of Community-Acquired Pneumonia

The definitive microbiologic etiology is determined in only 38%-63% of patients who develop community-
acquired pneumonia (CAP), depending on the patient population and diagnostic testing used. [1, 21]
Organisms have been traditionally classified as typical or atypical CAP pathogens depending on their
ability to be detected on Gram stain or standard bacterial cultures.
Typical community-acquired pneumonia pathogens
Typical bacterial pathogens that cause CAP include S pneumoniae, H influenza, and M catarrhalis (Gram
stains shown below). The frequency with which CAP is attributable to one of these pathogens varies
according to epidemiologic factors (eg, seasonality, patient demographics, exposure history) and the
diagnostic testing used. In the past, these organisms had been reported to account for most CAP cases. [22]
However, with improvement in diagnostic techniques allowing for better identification of viruses and
fastidious bacteria, our understanding of the etiologic agents involved in the development of CAP has
evolved. As a result, a smaller percentage of CAP cases are now being attributed to these typical bacterial
pathogens.

Gram stain showing Streptococcus pneumoniae.

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Gram stain showing Haemophilus influenzae.

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S pneumoniae remains the most common bacterial agent responsible for CAP. The incidence of S
pneumoniae pneumonia varies according to the population studied. A 2015 study of 267 patients with CAP
in Norway reported that S pneumoniae accounted for 30% of cases; this represented 48.5% of the cases in
which an organism was identified. [21] A separate study of adults with CAP in the United States identified S
pneumoniae as the etiologic agent in only 5% of total cases of CAP (13.5% of cases with an identified
pathogen). [1]

S aureus has not traditionally been considered a typical cause of CAP in otherwise healthy hosts. However,
S aureus is well known to cause potentially severe CAP after influenza infection. [3] In addition, community-
acquired methicillin-resistant S aureus (MRSA) has increasingly been associated with multilobar necrotizing
CAP, including in previously healthy individuals.

Importantly, K pneumoniae and Pseudomonas aeruginosa are not typical causes of CAP in otherwise
healthy hosts. K pneumoniae CAP occurs primarily in individuals with chronic alcoholism or diabetes
mellitus. P aeruginosa is a cause of CAP in patients with bronchiectasis or cystic fibrosis.

In certain patients admitted to the ICU, the microbial etiology of pneumonia may be complex. In a study by
Cilloniz et al, 11% of cases were polymicrobial. The most frequently identified pathogens in polymicrobial
infections were S pneumoniae, respiratory viruses, and P aeruginosa. Chronic respiratory disease and
acute respiratory distress syndrome (ARDS) criteria were independent predictors of a polymicrobial
infection. [23]

Other gram-negative pathogens (eg, Enterobacter species, Serratia species, Stenotrophomonas

maltophilia, Burkholderia cepacia) rarely cause CAP in patients without underlying lung disease or
immunosuppression.

Atypical community-acquired pneumonia pathogens

Atypical bacterial pneumonias can be differentiated into those caused by zoonotic or nonzoonotic atypical
pathogens.

Zoonotic atypical CAP pathogens include Chlamydophila (Chlamydia) psittaci (psittacosis), F tularensis
(tularemia), and C burnetii (Q fever).

Nonzoonotic atypical CAP pathogens include Legionella species (Legionnaires disease), M pneumoniae,
and C pneumoniae. [24]

Respiratory viruses are another important cause of atypical CAP. While certain viruses may be zoonotically
transmitted (eg, Hantavirus and avian influenza), most are transmitted person-to-person.

Epidemiology of Community-Acquired Pneumonia

Prevalence in the United States

The number of annual community-acquired pneumonia (CAP) cases is difficult to estimate. One study, in
which 46,237 elderly patients were monitored over a 3-year period, showed the rate of CAP among those
aged 65-69 years to be 18.2 cases per 1000 person-years. Among person older than 85 years, the rate was
52.3 cases per 1000 person-years. Estimates based on these data suggested that, annually, 1 of 20
persons older than 85 years develop CAP. The investigators also estimated that approximately 915,900
cases of CAP occur among elderly persons annually in the United States. [25, 26, 27]

In a more recent population-based surveillance study of CAP among adults presenting at one of 5 hospitals
in Chicago and Nashville, the annual incidence of CAP was estimated to be 24.8 cases (95% CI; 23.5-26.1)
per 10,000 adults. [1] The median age of patients presenting with CAP was 57 years (interquartile range, 46-
71 years). Similar to the prior studies, the incidence of CAP increased with age.

The prevalence and cost of CAP in 2011 in the United States Department of Veterans Affairs Hospitals was
examined, including 35,380 episodes of CAP among 7,824,850 veterans, or 452 cases per 100,000 person-
years. The estimated excess cost was $750,170,631, with over half incurred in patients older than 65 years.
[28]

International prevalence
A retrospective study using a nationwide claims database to determine the incidence of CAP in the
Netherlands identified 195,372 cases of CAP between 2008 and 2011. [29] This represented an average
incidence of 295 cases per 100,000 population per year. The authors concluded that the mean annual cost
of CAP in this population was 178 million euros, with a disproportionate amount (76%) of the cost being
incurred by people older than 50 years.

Age
Advanced age is associated not only with a higher incidence of CAP but also with more severe disease,
greater need for hospitalization, and higher mortality. [7, 30]

CAP encountered in the ambulatory setting is more common among young adults and is usually due to
atypical CAP pathogens (eg, Mycoplasma pneumoniae). [31]

Prognosis of Community-Acquired Pneumonia

Negative prognostic factors in community-acquired pneumonia (CAP) include preexisting lung disease,
underlying cardiac disease, poor splenic function, advanced age, multilobar involvement, and delayed
initiation of appropriate antimicrobial therapy. [32]

Extrapulmonary Findings in Atypical Community-Acquired

Pneumonia
Atypical community-acquired pneumonia (CAP) has classically been associated with more extrapulmonary
manifestations than typical bacterial CAP. However, there can be considerable overlap in the clinical
presentation of CAP due to various pathogens such that a definitive microbiologic diagnosis cannot be
made based on signs and symptoms alone. Certain constellations of findings in the setting of appropriate
historical clues may suggest an increased likelihood of a specific pathogen, thus warranting a targeted
investigation for that organism. A detailed review of all potential extrapulmonary findings in CAP is beyond
the scope of this article; however, some classic associations are included below:

M pneumoniae CAP is associated with the following findings: [33]

Headache, fever, malaise, sore throat in young adult with insidious onset of cough
Erythema multiforme major (Stevens-Johnson syndrome)
Cardiac conduction abnormalities
Hemolytic anemia and cold-agglutinin syndrome
Neurologic abnormalities, including aseptic meningitis or meningoencephalitis, Guillain-Barre
syndrome, transverse myelitis
Associated with epidemic outbreaks, eg, in schools or military barracks

Legionella pneumophila CAP (Legionnaires disease) is associated with the following findings: [34]

Gastrointestinal and neurologic symptoms in the setting of pneumonia

Positive history of waterborne exposure
Relative bradycardia during febrile episode
Hyponatremia, hypophosphatemia, elevated creatine phosphokinase (CPK) level, elevated ferritin
level, myoglobinuria
Leukocytosis with relative lymphopenia
Unresponsive to beta-lactam antibiotics
A case of Legionnaires disease from the Philadelphia outbreak, showing characteristics of relative bradycardia and
extrapulmonary involvement.
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This graph outlines a case of Legionella pneumonia, showing characteristics of bradycardia and extrapulmonary
involvement. Also shown is an initial lack of response to beta-lactam antibiotics, followed by effective treatment with
doxycycline.
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C burnetii CAP (Q fever) is associated with the following findings: [35, 36]

Acute infection
Severe retrobulbar headache, myalgias, fever, rigors, nonproductive cough
Elevated levels of transaminases and thrombocytopenia
Maculopapular or purpuric rash
Zoonotic exposure (goats, sheep, cattle most common)
Community-acquired pneumonia and shock
With the exception of CAP due to particularly virulent organisms (eg, MRSA, Hantavirus, severe acute
respiratory syndrome [SARS], Legionella), CAP does not typically present with shock in otherwise healthy
hosts. Therefore, in addition to considering the possibility of CAP due to a hypervirulent pathogen, patients
who present with fever, dyspnea, leukocytosis, pulmonary infiltrates, and shock in the absence of conditions
associated with hyposplenism should be evaluated for imitators of pneumonia, such as acute myocardial
infarction or acute pulmonary embolism.

Conditions that predispose to severe CAP should be considered in patients presenting with CAP and shock
in the absence of one of the aforementioned cardiopulmonary diseases. The following disorders and
therapies have been associated with severe CAP:

Chronic alcoholism
Amyloidosis
Chronic active hepatitis
Fanconi syndrome
Hyposplenism in elderly patients
Immunoglobulin A (IgA) deficiency
Intestinal lymphangiectasia
Myeloproliferative disorders
Waldenstrm macroglobulinemia
Non-Hodgkin lymphoma
Celiac disease
Regional enteritis
Szary syndrome
Congenital asplenia
Splenectomy
Sickle cell trait/disease
Splenic infarcts
Splenic malignancies
Corticosteroid therapy
Rheumatoid arthritis
Systemic lupus erythematosus ( SLE)
Systemic mastocytosis
Systemic necrotizing vasculitis

Patient History
Patients with community-acquired pneumonia (CAP) due to typical bacterial CAP pathogens typically
present with fever, dyspnea, and productive cough, often with pleuritic chest pain.

The clinical presentation of atypical CAP is more often subacute and associated with extrapulmonary
manifestations that may provide a clue to the etiology.

Zoonotic infection

Contact with the appropriate zoonotic vector or its by-product (eg, milk, urine, feces, placenta) is needed to
develop a zoonotic CAP. A history of occupational exposure to livestock (eg, farmers, veterinarians) or close
contact with a parturient animal should be sought in patients with suspected Q fever. Psittacosis is
preceded by recent contact with birds infected with C psittaci. Occupations and avocations associated with
increased risk include poultry farming, pet shops, veterinary clinics, and ownership of pet birds (classically
of the psittacine, or parrot, family). Hantavirus is transmitted via exposure to wild rodents, specifically to
aerosolized rodent urine or feces; thus, queries as to whether a patient presenting with severe CAP works
or recreates in a setting conducive to rodent exposure (eg, farms, ranches, forests) is warranted.

Physical Examination
Purulent sputum is characteristic of pneumonia caused by bacterial community-acquired pneumonia (CAP)
pathogens and is not usually a feature of pneumonia caused by atypical pathogens, with the exception of
Legionnaires disease. Blood-tinged sputum may be found in patients with pneumococcal pneumonia,
Klebsiella pneumonia, or Legionella pneumonia.

Rales are heard over the involved lobe or segment. Consolidation may be accompanied by an increase in
tactile fremitus, bronchial breathing, and egophony.

Legionella pneumonia, Q fever, and psittacosis are atypical pneumonias that may present with signs of
consolidation. Consolidation is not a typical feature of pneumonia caused by M pneumoniae or C
pneumoniae. [24]

Be wary when a patient presents with severe CAP, with or without hypotension or shock. In these patients,
be sure to exclude an underlying immunocompromise, asplenia, or acute pulmonary or cardiac event that
could explain the severity of the CAP.

Pleural effusion
Pleural effusion, if large enough, may be detectable on physical examination. In addition, patients with
pleural effusion also have decreased tactile fremitus and dullness on chest percussion.

Empyema

On physical examination, empyema has the same findings as pleural effusion.

Differential Diagnoses of Community-Acquired Pneumonia

Aside from those mentioned above, the differential diagnoses to consider in the diagnosis of community-
acquired pneumonia (CAP) include the following:

Acute bronchitis
Acute exacerbation of chronic bronchitis
Aspiration pneumonitis
Myocardial infarction
Congestive heart failure and pulmonary edema
Pulmonary fibrosis
Sarcoidosis
SLE pneumonitis
Pulmonary drug hypersensitivity reactions (nitrofurantoin)
Drug-induced pulmonary disease
Cryptogenic organizing pneumonia
Pulmonary embolus or infarction
Bronchogenic carcinomas
Radiation pneumonitis
Granulomatosis with polyangiitis (Wegener granulomatosis)
Lymphomas
Tracheobronchitis
Sputum Studies and Blood Culture
Send sputum samples from patients with community-acquired pneumonia (CAP) for Gram stain and/or
culture. Keep in mind that many patients, especially elderly persons, are not able to produce an adequate
suitable sputum sample.

Sputum Gram stain is reliable and diagnostic if performed on a well-collected specimen without many
squamous epithelial cells (saliva contamination) and if a predominant organism is present. Gram stain
shows few or no predominant organisms in patients with atypical CAP.

Obtain blood cultures from all patients with CAP upon admission because some bacterial pathogens, such
as S pneumoniae and H influenzae, are frequently associated with positive blood cultures. M catarrhalis
bacteremia is rare.

Studies in HIV-Positive Patients with Community-Acquired

Pneumonia
The differential diagnoses of community-acquired pneumonia (CAP) in patients with human
immunodeficiency virus (HIV) infection is broader than in HIV-negative patients. The patients immunologic
status, as reflected by the CD4 count, the clinical course, and the chest radiographic appearance, provides
clues to the most likely etiologic organism.

Patients with HIV infection and a normal or slightly decreased CD4 count with focal infiltrates have
approximately the same pathogen distribution as otherwise healthy hosts (eg, S pneumoniae is most
common) and thus warrant the same diagnostic strategies as the general population. Pneumocystis (carinii)
jiroveci pneumonia (PJP) should be suspected in patients with a CD4 count of less than 200 cells/L
presenting with gradually progressive dyspnea, nonfocal infiltrates on chest radiography, nonproductive
cough, and hypoxemia. A definitive diagnosis of PJP requires visualization of the P jirovecii cysts (ie, using
special stains such as Giemsa or methenamine silver); bronchoscopy with bronchoalveolar lavage (BAL) is
often necessary to obtain an adequate specimen.

Individuals with HIV infection are also at increased risk for active pulmonary tuberculosis; the radiographic
appearance of tuberculosis in HIV-infected patients varies, so tuberculosis should be considered in all
patients with HIV and a pulmonary infiltrate. Patients with HIV and CAP should therefore be placed on
airborne isolation (unless other etiology identified) until tuberculosis is excluded with three negative findings
on acid-fast bacillus (AFB) smears/sputum cultures.

Additional uncommon CAP pathogens, such as histoplasmosis, coccidioidomycosis, and cryptococcosis,

should also be considered in HIV-positive patients who present with pulmonary infiltrates, with risk stratified
according to potential exposure history. Antigen testing (urine antigen for histoplasmosis; serum antigen for
cryptococcosis) may be helpful in these cases.

Other Laboratory Tests for Community-Acquired Pneumonia

Several nonspecific laboratory tests are often performed during the workup of community-acquired
pneumonia (CAP), particularly if atypical CAP is suspected.

Serum transaminase, serum sodium, serum ferritin, serum phosphorus, and creatine phosphokinase (CPK)
levels may provide evidence supporting a particular pathogen, such as Legionella. C-reactive protein (CRP)
levels and procalcitonin may help predict the likelihood of a bacterial origin for CAP. Serum lactic acid, white
blood cell (WBC) count, blood urea nitrogen, and creatinine may be used in categorizing the severity of
illness.
Cold agglutinin titers of 1:32 or greater may support a diagnosis of M pneumoniae, however this test is
neither sensitive nor specific.

Procalcitonin and C-reactive protein levels

A prospective study of 75 children with CAP, including 37 who met the criteria for presumed pneumococcal
CAP (P-CAP), found procalcitonin (PCT) and CRP levels to be reliable markers of P-CAP. [37] High levels of
these markers were strongly associated with P-CAP. Whereas a PCT value of 0.5 ng/mL or lower ruled out
P-CAP in more than 90% of cases, a value of 1.5 ng/mL or higher in association with a positive
pneumococcal urinary antigen test result, yielded a diagnostic probability of almost 80% for P-CAP. [38]

Agglutinin levels
Cold-agglutinin antibodies (immunoglobulin M [IgM] autoantibodies directed against the erythrocyte)
develop in 50%-75% of patients with M pneumoniae infection, peaking approximately 2 weeks into the
illness. However, this finding is nonspecific, as low-titer cold-agglutinin elevations occur in various viral and
neoplastic illnesses. Furthermore, a negative cold agglutinin titer finding does not exclude Mycoplasma
infection.

Direct fluorescent antibody testing

Direct fluorescent antibody (DFA) testing of the sputum can be performed to try to assist with the diagnosis
of atypical CAP pathogens, including Legionella, P jiroveci, and Chlamydophila; however, the utility of this
test is hampered by suboptimal sensitivity and is relatively difficult to perform. A DFA stain showing
Legionella infection is seen in the image below.

Sputum direct fluorescent antibody stain showing Legionella infection.

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Serology

Serology can be useful in identifying fastidious organisms, particularly when dealing with pathogens with
potential epidemiologic implications (ie, epidemic or biohazard situations), such as B pertussis, M
pneumoniae, L pneumophila, or C burnetii. Serologic diagnosis is based on a 4-fold or greater increase in
titers between acute- and convalescent-phase serum specimens so is generally not useful in the acute-care
setting. A significantly elevated IgM titer (typically present in the acute phase of infection) may help support
a diagnosis, and some experts have suggested that combining IgM and nucleic acid amplification testing
may be the optimal method for diagnosing M pneumoniae infection. [39]
Urinary antigen test

Pneumococcal urinary antigen testing is a useful nonculture-based test for diagnosing pneumococcal
infection that has a reported sensitivity of 50%-80% and specificity of more than 90%. [40] Availability of the
assay is the main perceived barrier to its routine use. [40]

Urinary antigen testing is considered the first-line diagnostic test for L pneumophila. The sensitivity of the
test ranges from 55%-99%, with improved sensitivity paralleling disease severity. [34] The urinary antigen
test is applicable only for L pneumophila serogroup type I, which accounts for approximately 80% of
infections. The urinary antigen test remains positive for Legionella for long periods but may be negative
within the first 48 hours of infection.

Polymerase chain reaction

Polymerase chain reaction (PCR) has emerged as an important diagnostic tool for determining the etiology
of CAP, particularly with regard to respiratory viruses and fastidious organisms, including Legionella,
Mycoplasma, and Chlamydophila. [2] PCR is a very sensitive and specific method for isolating these
pathogens. The increasing commercial availability of various PCR assays (including multiplex) will allow for
increased implementation in the clinical setting. However, interpreting the isolation of organisms known to
colonize the upper airway or those that may be associated with protracted shedding, such as rhinovirus,
remains a challenge. Quantitative PCR methods have shown some promise in improving interpretability of
such findings. [41]

A 2016 study in the United Kingdom assessed the use of comprehensive molecular testing of a single lower
respiratory tract specimen to detect a pathogen in CAP. [42] The study compared (1) a combination of real-
time multiplex PCR assays targeting 26 different pathogens, including bacteria and viruses, with (2) culture-
based diagnostic testing of the same specimens. Quantification of bacterial load was performed for 8
common bacteria, including S pneumoniae, H influenzae, and M catarrhalis. A pathogen was detected in
87% of patients with CAP using the multiplex assay, whereas culture achieved a diagnosis in only 39% of
cases. Viruses were detected in 30% of cases. H influenzae and S pneumoniae were the most commonly
detected bacteria. Pathogen detection was not significantly decreased when a quantitative threshold for
detection of 105 CFU/mL for all bacterial loads was applied, although the mean bacterial load was lower in
patients who had received prior antibiotics than in those who had not. Interestingly, of the 268 patients who
received antibiotics prior to testing, 77.6% had a positive bacterial PCR finding, but only 32% were culture-
positive. The authors concluded that comprehensive molecular testing on a lower respiratory tract specimen
has the potential to positively affect targeted antibiotic therapy in most patients with CAP.

Chest Radiography and CT Scanning

Chest radiography

Obtain chest radiographs in all patients with suspected community-acquired pneumonia (CAP) to exclude
conditions that mimic CAP and to confirm the presence of an infiltrate compatible with the presentation of
CAP. [5, 6] (See the images below.)
Chest radiograph in a patient with HIV infection, bilateral perihilar infiltrates, and Pneumocystis jiroveci pneumonia.
View Media Gallery

Chest radiograph in a patient with HIV infection and focal infiltrates due to tuberculosis.
View Media Gallery

Chest radiography findings may be negative in patients who present very early with CAP. In these patients,
repeat chest radiography within 24 hours is recommended.

Chest radiography may assist with the differentiation of viral pneumonias from nonviral pneumonias. Viral
pneumonias tend to display few or no infiltrates on chest radiography, but, when infiltrates are present, they
are almost always bilateral, perihilar, symmetric, and interstitial.

Bacterial pneumonias have a predominantly focal segmental or lobar distribution, with or without pleural
effusions. Atypical bacterial pathogens have variable radiographic findings, ranging from focal segmental to
bilateral interstitial disease. P jiroveci (PJP) pneumonia typically manifests as bilateral patchy interstitial
infiltrates. Of note, radiographic findings alone are not reliable for differentiating specific etiologies of CAP.

Chest radiographic findings should be negative in patients with asthma or exacerbation of chronic bronchitis
who do not have CAP.

The infiltrates observed with congestive heart failure (CHF) appear as increased interstitial markings and
show vascular redistribution to the upper lobes. Patients with preexisting heart failure usually have
cardiomegaly.

Rapid cavitation is not a typical feature of CAP.

Community-acquired methicillin-resistant S aureus (CA-MRSA) CAP presents as a fulminant CAP with rapid
cavitation and necrotizing pneumonia caused by CA-MRSA (SCC mec IV) with the PVL gene, which
sometimes occurs after influenza.

Serial chest radiography can be used to observe the progression of CAP. Chest radiographic findings
worsen rapidly and require a significant period to improve. It is important to note that clinical resolution
occurs long before radiologic resolution.

CT scanning
Obtain a computed tomography (CT) scan of the chest when an underlying bronchogenic carcinoma is
suggested or if any abnormalities are not consistent with the diagnosis of pneumonia. Immunocompromised
patients may benefit from further narrowing of differential diagnoses with chest CT scanning.

Fine-Needle Aspiration, Transtracheal Aspiration, and

Bronchoscopy With Bronchoalveolar Lavage
Diagnostic bronchoscopy with bronchoalveolar lavage (BAL) may be useful in patients with community-
acquired pneumonia (CAP) when Pneumocystis, mycobacteria, or fungal pathogens are likely. Diagnostic
bronchoscopy with BAL with or without biopsy may also be useful in unresolving CAP that does not respond
to appropriate therapy.

Transthoracic fine-needle aspiration (FNA) of the infiltrate can be performed and is most useful in
determining the cause of nodules or noninfection-associated infiltrates that are not responding to antibiotic
treatment.

Transtracheal aspiration (TTA) is a potentially hazardous procedure and offers no additional diagnostic
information in patients with CAP.

Histologic Findings
Lung sections with typical bacterial pneumonias show the progression from red hepatization to white
hepatization during the resolution process. The lung is repaired or scarred after bacterial pneumonia is
complete and the infectious process resolves.

Hospital Care in Community-Acquired Pneumonia

Although patients with mild community-acquired pneumonia (CAP) may be treated in an ambulatory setting,
patients with CAP who are moderately to severely ill should be hospitalized. Patients with severe CAP
require admission to an intensive care unit (ICU). Oxygen and/or ventilatory support may be required. [18, 43,
44, 45, 46, 47]
Because the severity of CAP is frequently due to underlying chronic disease, provide evidence-based
sepsis management while administering antibiotics for CAP.

Patients admitted with severe CAP and hypotension or shock are often hypotensive because of sepsis.

If no acute cardiopulmonary explanation can be found (eg, exacerbation of severe underlying lung disease,
exacerbation of preexisting CHF), patients with shock likely have diminished or absent splenic function or
immunocompromise.

Pharmacologic Therapy
There is no optimal therapy for community-acquired pneumonia (CAP). Most experts feel that coverage
should be divided against typical and atypical CAP pathogens. [48] Excellent practice guidelines have been
promulgated by the Infectious Diseases Society of America (IDSA) and the American Thoracic Society
(ATS). These resources provide evidence-based guidelines for the treatment of outpatients, inpatients, and
ICU patients with CAP. [7]

Adequate therapy for CAP includes coverage for S pneumoniae and atypical bacterial pathogens.
Treatment options for CAP in outpatients with no comorbidities and no risk factors for drug-resistant S
pneumoniae include the following: [7]

A macrolide (azithromycin, clarithromycin or erythromycin)

Doxycycline

Treatment options in patients with comorbidities such as chronic heart, lung, liver or renal disease; diabetes
mellitus; alcoholism; malignancy; asplenia; immunosuppression; prior antibiotics within 90 days; or other
risk for drug resistant infection include the following:

Respiratory fluoroquinolones (moxifloxacin, levofloxacin)

Beta-lactam (high-dose amoxicillin 1 g three times/day) or amoxicillin/clavulanate (2 g twice a day), or
ceftriaxone, cefpodoxime, or cefuroxime (500 mg twice daily) plus a macrolide or doxycycline

In regions with high rates of macrolide-resistant S pneumoniae, consider a nonmacrolide alternative.

In hospitalized patients, therapy consists of the following:

Beta-lactam (ceftriaxone) plus a macrolide or

Respiratory fluoroquinolone

Recent studies have suggested that the use of a beta-lactam alone may be noninferior to a beta-
lactam/macrolide combination or fluoroquinolone therapy in hospitalized patients. [9]

Therapy in ICU patients includes the following:

Beta-lactam (ceftriaxone, cefotaxime, or ampicillin/sulbactam) plus either a macrolide or respiratory

fluoroquinolone
For patients with penicillin allergy, a respiratory fluoroquinolone and aztreonam

Patients who are severely ill or unable to tolerate or absorb oral medications require a longer duration of
intravenous therapy before switching to an oral antibiotic. [15] If Pseudomonas is suspected, an
antipseudomonal beta-lactam (piperacillin/tazobactam, cefepime, imipenem, or meropenem) plus
ciprofloxacin or levofloxacin is recommended. If MRSA is suspected, vancomycin or linezolid is
recommended. For patients with penicillin allergy, aztreonam is used instead of the beta-lactam in the
regimen listed above.
Mild to moderately ill patients with CAP may be treated entirely via the oral route, on either an inpatient or
outpatient basis. Patients receiving oral antibiotics may be admitted for hospital services (eg, pulmonary
toilet and additional diagnostic tests) that are not obtainable on an outpatient basis.

If the patient is switched to an oral regimen and is doing well, earlier discharge from the hospital is possible.
The oral therapy regimen can be completed at home. Optimal intravenous-to-oral switch therapy consists of
a single agent that has an appropriate spectrum, has excellent bioavailability, is well tolerated, has a low
resistance potential, and is relatively inexpensive.

The duration of therapy for uncomplicated CAP is approximately 5-7 days. [7, 10] Patients should be afebrile
48-72 hours and have no signs of instability before antibiotic therapy is stopped. The duration of therapy
may need to be longer if initial empiric therapy did not have activity against the detected pathogen. Very
healthy young adults and children may be treated for shorter periods.

The use of systemic corticosteroids in patients with CAP may reduce the length of time until clinical stability,
reduce hospital length of stay, reduce the need for mechanical ventilation, and reduce the incidence of adult
respiratory distress syndrome (ARDS). [49, 50] Recent clinical trials have also shown a possible overall
reduction in mortality, although these later results remain in doubt. [51, 52] Furthermore, there is insufficient
data or agreement on the dose or duration of the steroid therapy. Adverse effects noted in the studies have
included hyperglycemia. [49] There are current ongoing double-blind, randomized, controlled clinical trials to
examine the short- and long-term effects of corticosteroid use in the management of CAP. [50]

Comorbid conditions
Comorbid conditions do not affect the selection of antimicrobial therapy. The addition and/or change of
antibiotics based on the severity of illness and/or comorbidities makes little sense. Antimicrobial therapy is
directed against the pathogen rather than against the comorbid factors. Comorbidities are an important
prognostic factor and contribute to the severity index. [32]

Severity

The severity of CAP may be estimated with scoring systems that consider age, end organ damage
manifested as uremia and/or confusion, respiratory rate, and blood pressure (CURB-65).

Other scoring systems include the Pneumonia Severity Index (PSI), SMART-COP, A-DROP, and expanded
CURB-65 (see Hospital admission). Prognosis is significantly affected by underlying conditions of the lungs,
heart, and spleen.

Appropriate spectrum
In otherwise healthy hosts with CAP, therapy does not need to cover S aureus, Klebsiella species, or P
aeruginosa. S aureus coverage should be included in patients with influenza who have focal infiltrates.

Most antibiotics used to treat community-acquired aspiration pneumonia (eg, beta-lactam/beta-lactamase

inhibitor) are highly effective against oral anaerobes. Metronidazole and clindamycin are unnecessary
unless anaerobic lung infection is suspected. For aerobic lung abscesses, clindamycin or moxifloxacin is
preferable. [53, 54, 55, 56] Coverage should include typical (S pneumoniae, H influenzae, M catarrhalis) and
atypical (Legionella and Mycoplasma species, C pneumoniae) pathogens.

Monotherapy

Monotherapy coverage of typical and atypical pathogens in CAP is preferred over double-drug therapy;
monotherapy is less expensive than double-drug regimens, while being as effective. [57]

Preferred monotherapy for CAP includes doxycycline or a respiratory quinolone. This is the most cost-
effective way to optimally treat CAP. It is well-tolerated in oral and intravenous forms. It is ideal for
intravenous-to-oral switch monotherapy in terms of patient compliance, safety, and cost. [58, 59]

Penicillin resistance
Most penicillin-resistant S pneumoniae infections may also be treated with beta-lactams. Alternately,
doxycycline or respiratory quinolones may be used. Vancomycin is rarely, if ever, needed.

High-level penicillin-resistant S pneumoniae (MIC 6 g/mL) strains are a rare cause of CAP, although they
remain susceptible to ceftriaxone.

Proton-pump inhibitors
Avoid using proton-pump inhibitors (PPIs) in combination with respiratory quinolones for CAP drug therapy.
The PPI should be discontinued or replaced with a histamine-2 (H2) blocker for the duration of therapy.
However, there is conflicting evidence as to the safety of using PPIs and H2 blockers. [60, 61, 62, 63]

Eurich et al concluded that acid suppressants substantially increase the risk of recurrent pneumonia in high-
risk elderly patients. In a cohort of elderly patients who had previously been hospitalized for pneumonia, the
investigators studied PPI and H2 blocker use during 5.4 years of follow-up, matching 248 patients with
recurrent pneumonia with 2476 controls. [60] Patients in the study who were currently using PPI/H2 blocker
had a higher rate of recurrent pneumonia than did nonusers (12% vs 8%, respectively).

In contrast, a population-based, nested case-control study by Dublin et al concluded that PPIs and H2
blockers do not increase the risk of pneumonia in older adults. [62]

Compared with H2 blockers, PPIs were associated with an increased risk of C difficile colitis. [64]

Outpatient Care in Community-Acquired Pneumonia

Monitor patients with mild community-acquired pneumonia (CAP) who are being treated on an outpatient
basis to ensure compliance with their medications and improvement. After 1 week, a repeat visit is
advisable. If the patient is improving and parapneumonic complications are not evident, posttherapy chest
radiography is unnecessary. [65, 66, 67]

The diet in patients with CAP is as tolerated. Guide activity with common sense.

Vaccination
Pneumococcal vaccines have been shown to have some efficacy in preventing vaccine-strain
pneumococcal pneumonia, bacteremia, and invasive disease. They have not been shown to prevent
community-acquired pneumonia (CAP) of all kinds. [68, 69] Annual influenza vaccination has been shown to
decrease pneumonia diagnoses, hospitalizations, and cardiac events in certain populations. [70, 71, 72, 73]

Annual influenza vaccination is recommended in all persons older than 6 months. The options for
vaccination include the trivalent inactivated vaccine, the quadrivalent inactivated vaccine, the live
attenuated intranasal quadrivalent vaccine, the trivalent inactivated cell culture vaccine, and the trivalent
inactivated recombinant vaccine. The live attenuated nasal spray is approved for patients aged 2-49 years
who are not pregnant, children receiving aspirin therapy, immunosuppressed persons, children with asthma
in the past 12 months, individuals receiving antiviral medications, and caretakers of immunocompromised
persons. Persons aged 18 years or older with egg allergy are eligible for the recombinant vaccine, which
should be administered by a physician experienced in the management of allergic conditions. People with
severe allergy to the flu vaccine should not receive it, and persons with history of Guillain-Barr syndrome
should consult with their physician prior to being vaccinated. [74]

Two pneumococcal vaccines are approved in the United States; 13-valent polysaccharide conjugate
vaccine (PCV13; Prevnar 13) is approved for children aged 6 weeks to 17 years and adults aged 50 years
or older. The 23-valent pneumococcal polysaccharide vaccine (PPSV23; Pneumovax 23) is approved for
adults aged 65 years or older and persons aged 2 years or older who are at increased risk for
pneumococcal disease.

On February 1, 2016, the Advisory Committee on Immunization Practices (ACIP) published updated
recommendations for pneumococcal vaccination in adults. The committee now recommends routine use of
PCV13 in addition to PPSV23 for adults older than 65 years. It is recommended that an initial dose of
PCV13 be given, followed by PPSV23 at least one year later. If PPSV23 has already been given, it should
be followed by PCV13 a year later. A second dose of PPSV23 is not needed in immunocompetent hosts. If
PPSV23 is inadvertently given prior to 1 year after PCV13, it does not need to be repeated.

In adults aged 19 years and older with immunocompromising conditions (eg, HIV, cancer, renal disease),
functional or anatomic asplenia, cerebrospinal fluid leaks, or cochlear implants, it is recommended that they
receive PCV13, followed by PPSV23 at least 8 weeks later. In patients who have previously received
PPSV23 vaccine, administer 1 dose of PCV13 at least 1 year after the last PPSV23 dose. A second dose of
PPSV23 is recommended 5 years after the first dose in persons in this category aged 19-64 years. If the
first dose of PPSV23 was administered prior to age 65 years, an additional dose should be administered at
age 65 years or at least 5 years after the prior dose. Subsequent doses of PPSV23 should not be given
sooner than 8 weeks after a dose of PCV13 and 5 years after the most recent dose of PPSV23. [75]

Nonleukopenic compromised hosts, such as those with rheumatoid arthritis, SLE, or alcoholism, may not
develop an antibody response to the pneumococcal vaccine and may therefore remain susceptible to
pneumococcal pneumonia. The same is true concerning the use of the Haemophilus vaccine.

Patient Instructions
Remind patients with community-acquired pneumonia (CAP) to comply with the medication even after they
experience clinical improvement. Except in patients with heart failure, adequate hydration and preservation
of the cough reflex during the convalescent period are important.

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Media Gallery

Gram stain showing Streptococcus pneumoniae.

Gram stain showing Haemophilus influenzae.
Gram stain showing Moraxella catarrhalis.
Clinical diagnostic approach in community-acquired pneumonias.
Sputum direct fluorescent antibody stain showing Legionella infection.
A case of Legionnaires disease from the Philadelphia outbreak, showing characteristics of relative
bradycardia and extrapulmonary involvement.
 This graph outlines a case of Legionella pneumonia, showing characteristics of bradycardia and
extrapulmonary involvement. Also shown is an initial lack of response to beta-lactam antibiotics,
followed by effective treatment with doxycycline.
Chest radiograph in a patient with HIV infection, bilateral perihilar infiltrates, and Pneumocystis jiroveci
pneumonia.
Chest radiograph in a patient with HIV infection and focal infiltrates due to tuberculosis.

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Contributor Information and Disclosures

Author

Stephanie L Baer, MD Assistant Professor of Medicine, Division of Infectious Diseases, Department of

Medicine, Medical College of Georgia, Georgia Regents University; Chief, Epidemiology and Infection
Control, Charlie Norwood VA Medical Center

Stephanie L Baer, MD is a member of the following medical societies: American Federation for Medical
Research, Infectious Diseases Society of America, Society for Healthcare Epidemiology of America

Disclosure: Received research grant from: Pfizer.

Coauthor(s)

Rhonda E Colombo, MD, MHS Assistant Professor of Medicine, Director, Infectious Diseases Fellowship
Program, Department of Medicine, Division of Infectious Diseases, Medical College of Georgia, Georgia
Regents University

Rhonda E Colombo, MD, MHS is a member of the following medical societies: American College of
Physicians, American Federation for Medical Research, Infectious Diseases Society of America, Southern
Society for Clinical Investigation

Disclosure: Nothing to disclose.

Jose A Vazquez, MD, FACP, FIDSA Professor of Medicine, Chief, Division of Infectious Diseases,
Department of Medicine, Medical College of Georgia at Augusta University

Jose A Vazquez, MD, FACP, FIDSA is a member of the following medical societies: American College of
Physicians, American Society for Microbiology, HIV Medicine Association, Immunocompromised Host
Society, Infectious Diseases Society of America, International AIDS Society, International
Immunocompromised Host Society, International Society for Human and Animal Mycology, International
Society for Infectious Diseases, Medical Mycological Society of the Americas, Michigan Infectious Disease
Society, Mycological Society of America, National Foundation for Infectious Diseases

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Allergan; Astellas<br/>Received

research grant from: Merck; Astellas<br/>Received grant/research funds from Merck for independent
contractor; Received honoraria from Forest for speaking and teaching; Received honoraria from Astellas for
speaking and teaching; Received consulting fee from Cidara for consulting.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor
of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New
Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at
New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: American College of Physicians,
Alliance for the Prudent Use of Antibiotics, The Foundation for AIDS Research, Southern Society for
Clinical Investigation, Southwestern Association of Clinical Microbiology, Association of Professors of
Medicine, Association for Professionals in Infection Control and Epidemiology, American Clinical and
Climatological Association, Infectious Disease Society for Obstetrics and Gynecology, Orleans Parish
Medical Society, Southeastern Clinical Club, American Association for the Advancement of Science, Alpha
Omega Alpha, American Association of University Professors, American Association for Physician
Leadership, American Federation for Medical Research, American Geriatrics Society, American Lung
Association, American Medical Association, American Society for Microbiology, American Thoracic Society,
American Venereal Disease Association, Association of American Medical Colleges, Association of
American Physicians, Infectious Diseases Society of America, Louisiana State Medical Society, Royal
Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southern Medical Association

Disclosure: Received royalty from Baxter International for other.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart
G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health
Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of
America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American
Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation,
Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of
America

Disclosure: Nothing to disclose.

Additional Contributors

Fred A Lopez, MD Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for
Student Affairs, Louisiana State University School of Medicine

Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College
of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, Louisiana
State Medical Society

Disclosure: Nothing to disclose.

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony
Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians,
American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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