Community-Acquired Pneumonia (CAP)

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 patient’s

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