INTRODUCTION — Childhood pneumonia is an important cause of morbidity in the developed world,

and morbidity and mortality in the developing world. The epidemiology, microbiology, and
pathogenesis of pneumonia in children will be reviewed here. The clinical features, diagnosis, and
treatment of pneumonia in children are discussed separately, as is pneumonia in neonates (<28 days
of age). (See "Clinical features and diagnosis of community-acquired pneumonia in
children" and "Outpatient treatment of community-acquired pneumonia in children" and "Inpatient
treatment of pneumonia in children" and "Neonatal pneumonia".)

TERMINOLOGY — The terms pneumonia and pneumonitis strictly represent any inflammatory
condition involving the lungs, which include the visceral pleura, connective tissue, airways, alveoli, and
vascular structures. Lower respiratory tract infection (LRTI) is frequently used interchangeably to
include bronchitis, bronchiolitis, and pneumonia, or any combination of the three. For the purposes of
this review, pneumonia will be defined as a condition typically associated with fever, respiratory
symptoms, and evidence of parenchymal involvement, either by physical examination or the presence
of infiltrates on chest radiography. Bronchiolitis is discussed separately. (See "Bronchiolitis in infants
and children: Clinical features and diagnosis", section on 'Clinical features' .)

EPIDEMIOLOGY

Incidence — The World Health Organization (WHO) estimates there are 156 million cases of
pneumonia each year in children younger than five years, with as many as 20 million cases severe
enough to require hospital admission [ 1 ]. In the developed world, the annual incidence of pneumonia
is estimated to be 33 per 10,000 in children younger than five years and 14.5 per 10,000 in children 0
to 16 years [ 2 ].

Approximately one-half of children younger than five years of age with community-acquired pneumonia
(CAP) require hospitalization [ 3 ]. Hospitalization rates for pneumonia (all causes) among children
younger than two years in the United States decreased after introduction of the pneumococcal
conjugate vaccine to the routine childhood immunization schedule in 2000 (from 12 to 14 per 1000
population to 8 to 10 per 1000 population) ( figure 1 ) [ 4 ].

Mortality — The mortality rate in developed countries is low (<1 per 1000 per year) [ 5 ]. In
developing countries, respiratory tract infections are not only more prevalent but more severe,
accounting for more than 2 million deaths annually; pneumonia is the number one killer of children in
these societies [ 1,6 ].

Seasonality — Although both viral and bacterial pneumonia occur throughout the year, they are
more prevalent during the colder months, presumably because direct transmission of infected droplets
is enhanced by indoor crowding. For reasons that are unknown, different viruses cause peaks of
infection at different times during the respiratory virus season and these peaks seldom occur
simultaneously [ 7 ]. In tropical regions, peaks of infection follow no common pattern and can occur
during either the wet or dry seasons.

Risk factors — Most studies have shown that pediatric lower respiratory tract infection (LRTI),
including pneumonia, are more frequent in boys, with a male-female ratio of 1.25:1 to 2:1 [ 8 ]. Lower
socioeconomic groups have a higher prevalence of LRTIs, which correlates best with family size, a
reflection of environmental crowding. School-age children often introduce respiratory viral agents into
households, resulting in secondary infections in their parents and siblings [ 7 ].

Underlying cardiopulmonary disorders and other medical conditions predispose to pneumonia and
contribute to increasing severity. These include [ 5,9 ]:

 Congenital heart disease

 Bronchopulmonary dysplasia
 Cystic fibrosis
 Asthma
 Sickle cell disease
 Neuromuscular disorders, especially those associated with a depressed consciousness
  Some gastrointestinal disorders (eg, gastroesophageal reflux, tracheoesophageal fistula)
 Congenital and acquired immunodeficiency disorders

Cigarette smoke compromises natural pulmonary defense mechanisms by disrupting both mucociliary
function and macrophage activity [ 10 ]. Exposure to cigarette smoke, especially if the mother smokes,
increases the risk for pneumonia in infants younger than one year of age. (See "Secondhand smoke
exposure: Effects in children" .)

The use of cigarettes, alcohol, and other substances of abuse in adolescents may increase the risk of
pneumonia by increasing the risk of aspiration through impairment of the cough and epiglottic reflexes.
In addition, the use of alcohol has been associated with increased colonization of the oropharynx with
aerobic gram-negative bacilli [ 11 ].

Effect of vaccines — Immunization with the Haemophilus influenzae type b (Hib) and pneumococcal
conjugate vaccines protects children from invasive disease caused by these organisms. Hib was once a
common cause of pneumonia in young children in the United States. However, it has been virtually
eliminated as a result of routine immunization with Hib conjugate vaccines.

The universal immunization of infants in the United States with the 7-valent pneumococcal conjugate
vaccine has effectively decreased the incidence of pneumonia requiring hospitalization and other
invasive Streptococcus pneumoniae infections in children younger than two years ( figure 1 ) [ 12,13 ].
Rates of ambulatory visits for pneumonia in children younger than two years also declined after the
introduction of pneumococcal conjugate vaccine [ 14 ], but the rates for children aged 1 to 18 years
remained stable [ 15 ]. (See "Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in
children", section on 'Pneumonia' .)

It is anticipated that the 13-valent pneumococcal conjugate vaccine that replaced the 7-valent
pneumococcal conjugate vaccine in 2010 and affords additional coverage against serotypes 1, 3, 5, 6A,
7F, and 19A will further decrease the incidence of pneumonia requiring hospitalization because these
serotypes currently are responsible for the majority of pneumococcal pneumonia cases among children
worldwide [ 16,17 ]. (See "Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children",
section on '13-valent vaccine' .)

Pneumococcal vaccination also protects against viral pneumonia. This was shown in a double-blind,
randomized, placebo-controlled trial in which full immunization with a nine-valent pneumococcal
conjugate vaccine was associated with a 31 percent reduction (95% CI 15-43) in the incidence of
pneumonia associated with any of seven respiratory viruses (influenza, parainfluenza, respiratory
syncytial virus (RSV), adenovirus) in hospitalized children [ 18 ]. This observation suggests that the
pneumonias associated with these viruses in hospitalized children are often because of concurrent
pneumococcal infection.

PATHOGENESIS — Pneumonia occurs because of an impairment of host defenses, invasion by a

virulent organism, and/or invasion by an overwhelming inoculum.

In the typical scenario, pneumonia follows an upper respiratory tract illness that permits invasion of
the lower respiratory tract by bacteria, viruses, or other pathogens that trigger the immune response
and produce inflammation [ 3,19 ]. The lower respiratory tract air spaces fill with white blood cells
(WBC), fluid, and cellular debris. This process reduces lung compliance, increases resistance, obstructs
smaller airways, and may result in collapse of distal air spaces, air trapping, and altered ventilation-
perfusion relationships [ 3 ]. Severe infection is associated with necrosis of bronchial or bronchiolar
epithelium [ 20 ].

Acquisition — The agents that cause lower respiratory tract infection (LRTI) are most often
transmitted by droplet spread resulting from close contact with a source case. Contact with
contaminated fomites also may be important in the acquisition of viral agents, especially respiratory
syncytial virus (RSV).

Most typical bacterial pneumonias are the result of initial colonization of the nasopharynx followed by
aspiration or inhalation of organisms. Invasive disease most commonly occurs upon acquisition of a
new serotype of the organism with which the patient has not had previous experience, typically after
an incubation period of one to three days. Occasionally, a primary bacteremia may precede the
pneumonia. Atypical bacterial pathogens attach to respiratory epithelial membranes through which
they enter cells for replication.

The viral agents that cause pneumonia proliferate and spread by contiguity to involve lower and more
distal portions of the respiratory tract.

Normal host defense — The pulmonary host defense system is complex and includes anatomic and
mechanical barriers, humoral immunity, phagocytic activity, and cell-mediated immunity [ 8,21,22 ],
as discussed below, with a focus on bacterial infection. The host response to respiratory viral infection
is beyond the scope of this review; more information can be obtained from reference [ 23 ].

 Anatomic and mechanical barriers – Anatomic and mechanical barriers in the upper airway
comprise an important part of the host defense. Particles greater than 10 microns are efficiently
filtered by the hairs in the anterior nares or impact onto mucosal surfaces. The nasal mucosa
contains ciliated epithelium and mucus-producing cells. The cilia beat synchronously, clearing
the entrapped organisms through the nasopharynx via expulsion or swallowing. In the
oropharynx, salivary flow, sloughing of epithelial cells, local production of complement and IgA,
and bacterial interference from the resident flora serve as important factors in local host
defense.

An intact epiglottic reflex helps to prevent aspiration of infected secretions, and the cough reflex
helps to expel materials that may be aspirated. The sharp angles at which the central airways
branch cause 5 to 10 micron particles to impact on mucosal surfaces, where they are entrapped
in endobronchial mucus. Once entrapped, the ciliary system moves the particles upward out of
the airways into the throat, where they are normally swallowed.
 Humoral immunity – Secretory IgA is the major immunoglobulin produced in the upper airways
and accounts for 10 percent of the total protein concentration of nasal secretions. Although it is
not a very good opsonizing agent, it does possess antibacterial and antiviral activity. IgG and
IgM enter the airways and alveolar spaces predominantly via transudation from the blood and
act to opsonize bacteria, activate complement, and neutralize toxin. Immunoglobulins,
surfactant, fibronectin, and complement act as effective opsonins to help eliminate
microorganisms (0.5 to 1 micron particles) that reach the terminal airways and alveoli. Free
fatty acids, lysozyme, and iron-binding proteins also are present and may be microbicidal.
 Phagocytic cells – There are two populations of phagocytic cells in the lung: polymorphonuclear
leukocytes (PMNs) from the blood and macrophages. There are several distinct populations of
macrophages, which vary in their location and function:

 The alveolar macrophage is located in the alveolar fluid and is the first phagocyte encountered
by inert particles and potential pathogens entering the lung. If this cell is overwhelmed, it has
the capacity to become a mediator of inflammation and produce cytokines that recruit
neutrophils.
 Interstitial macrophages are located in the lung connective tissue and serve both as phagocytic
cells and antigen-processing cells.
 The intravascular macrophage is located in capillary endothelial cells and phagocytizes and
removes foreign material entering the lungs via the bloodstream.

 Cell-mediated immunity – Cell-mediated immunity is especially important against certain

pathogens, including viruses and intracellular microorganisms that can survive within pulmonary
macrophages. Although relatively few in number (5 to 10 percent of the total lung parenchyma
cell population), lymphocytes play three critical roles: the production of antibody, cytotoxic
activity, and the production of cytokines.

Patterns of pneumonia — There are five patterns of bacterial pneumonia [ 19 ]:

 Lobar pneumonia – involvement of a single lobe or segment of a lobe; this is the classic pattern
of S. pneumoniae pneumonia
 Bronchopneumonia – primary involvement of airways and surrounding interstitium; this pattern
is sometimes seen in Streptococcus pyogenes andStaphylococcus aureus pneumonia
  Necrotizing pneumonia (associated with aspiration pneumonia and pneumonia resulting from S.
pneumoniae , S. pyogenes , and S. aureus ) ( image 1 )
 Caseating granuloma (as in tuberculosis pneumonia)
 Interstitial and peribronchiolar with secondary parenchymal infiltration – this pattern typically
occurs when a severe viral pneumonia is complicated by bacterial pneumonia

There are two patterns of viral pneumonia [ 19 ]:

 Interstitial pneumonitis ( image 2 )

 Parenchymal infection with viral inclusions

Examination findings — The examination findings vary depending on the site of infection as follows
[ 3 ]:

 Inspiratory crackles, also called rales and crepitations [ 24 ], are more common in lobar
pneumonia and bronchiolitis/pneumonia
 Decreased breath sounds may be noted in areas of consolidation
 Coarse, low-pitched continuous breath sounds (rhonchi) are more common in
bronchopneumonia
 Expiratory wheezes, high-pitched breath sounds, are caused by oscillation of air through a
narrowed airway; they are more common in bronchiolitis and interstitial pneumonitis

ETIOLOGIC AGENTS — A large number of microorganisms have been implicated as etiologic agents
of pneumonia in children ( table 1A-B ). The agents commonly responsible vary according to the age of
the child and the setting in which the infection is acquired.

Community-acquired pneumonia

Overview — The true prevalence of the various etiologic agents in community-acquired pneumonia
(CAP) in children is uncertain [ 25 ]. Studies investigating the etiology of childhood pneumonia have
been performed in populations of various ages, in various settings, and using a variety of microbiologic
techniques [ 26-37 ]. Because direct culture of infected lung tissue requires invasive techniques,
published studies primarily use laboratory tests that provide indirect evidence of etiology. These
indirect methods include nasopharyngeal culture, blood culture, polymerase chain reaction, and
serology. In addition to the use of indirect methods, interpretation of the results is hampered by the
failure to identify an organism in 15 to 35 percent of cases and the frequency of mixed infections (in 23
to 33 percent of cases) [ 2 ]. Most of these studies were performed before the licensure of the
pneumococcal conjugate vaccine [ 38 ].

Despite these problems, systematic reviews have identified some consistent trends and conclusions
regarding the etiology of CAP in children, which are listed below [ 2,25 ]:

 S. pneumoniae is the most common bacterial cause of pneumonia in children [ 9,39 ]

 Viruses alone account for 14 to 35 percent of cases, and up to 50 percent of cases in young
children
 Viruses are more commonly identified in children younger than five years
 In children older than five years, Mycoplasma pneumoniae ,
and Chlamydophila (formerly Chlamydia ) pneumoniae are more common [ 40,41 ]

In some areas in which community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA)

is a major issue, CA-MRSA is becoming an important cause of CAP complicated by empyema and
necrosis [ 42,43 ]. When associated with influenza, MRSA CAP can be particularly severe [ 44,45 ].
(See "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and empyema in
children" and "Clinical features and diagnosis of seasonal influenza in children", section on 'Bacterial
coinfection' and "Epidemiology and clinical spectrum of methicillin-resistant Staphylococcus aureus
infections in children", section on 'Epidemiology and risk factors' .)

In neonates — The etiology of pneumonia in neonates (infants <28 days of age) is discussed
separately. (See "Neonatal pneumonia", section on 'Microbiology'.)
In infants — As described below, viruses are the most common etiology of CAP in children younger
than five years, including infants. However, infants younger than one year also may develop "afebrile
pneumonia of infancy." Afebrile pneumonia of infancy is a syndrome generally seen between two
weeks and three to four months of life. It is classically caused by Chlamydia trachomatis , but other
agents, such as cytomegalovirus (CMV), Mycoplasma hominis , and Ureaplasma urealyticum , also are
implicated. (See "Chlamydia trachomatis infections in the newborn", section on 'Pneumonia' .)

Infants with severe Bordetella pertussis infection also may develop pneumonia. (See "Clinical features
and diagnosis of Bordetella pertussis infection in infants and children", section on 'Complications' .)

In children <5 years

 Viruses – Viruses are the most common etiology of CAP in older infants and children younger
than five years of age [ 2,25 ]. However, bacterial pathogens, including S. pneumoniae , S.
aureus , and S. pyogenes , also are important because they are associated with increased
morbidity and mortality [ 43,44,46 ].

Respiratory syncytial virus (RSV), a member of the Paramyxoviridae virus family, is the most
common viral pathogen responsible for pneumonia in children younger than five years [ 32 ].
RSV pneumonia frequently represents an extension of bronchiolitis. (See "Bronchiolitis in infants
and children: Clinical features and diagnosis", section on 'Clinical features' and "Respiratory
syncytial virus infection: Clinical features and diagnosis", section on 'Clinical manifestations' .)

Other viral causes of pneumonia in children younger than five years include:

 Influenza A and B viruses. (See "Clinical features and diagnosis of seasonal influenza in
children", section on 'Pneumonia' .)
 Parainfluenza viruses, usually type 3. (See "Parainfluenza viruses in children", section on
'Clinical presentation' .)
 A number of adenovirus serotypes (1, 2, 3, 4, 5, 7, 14, 21, and 35) have been reported to
cause pneumonia; serotypes 3, 7, and 21 have been associated with severe and complicated
pneumonia [ 47 ]. (See "Epidemiology and clinical manifestations of adenovirus infection",
section on 'Clinical presentation' .)
 Human metapneumovirus, identified in 2001, is a common cause of lower respiratory tract
infections in children; most children have been infected by five years of age. (See "Human
metapneumovirus infections" .)
 Rhinovirus has been implicated as a cause of pneumonia using PCR assays [ 48 ], but its
etiologic role is questioned [ 49 ].
 Coronaviruses, including the severe acute respiratory syndrome (SARS) virus and the New
Haven coronavirus, also cause respiratory tract infections in children younger than five years
[ 50 ]. However, their clinical impact has yet to be fully determined [ 51 ]. (See "Severe acute
respiratory syndrome (SARS)"and "Coronaviruses" .)
 Human bocavirus and human parechovirus types 1, 2, and 3 also have been implicated as a
cause of lower respiratory tract infections in children [ 52-54 ].

 Bacteria – Important bacterial causes of pneumonia in preschool children include S.

pneumoniae , H. influenzae type b , nontypeable H. influenza , Moraxella catarrhalis , S.
aureus , S. pyogenes , and atypical bacteria.

 S. pneumoniae is the single most common bacterial pathogen causing pneumonia in all patients
beyond the first few weeks of life [ 9,39 ]. (See"Pneumococcal pneumonia in children", section
on 'Epidemiology' .)
 H. influenzae type b is a rare cause of pneumonia in countries with universal childhood
immunization.
 S. aureus (particularly community-associated MRSA, CA-MRSA) and S. pyogenes are becoming
increasingly frequent causes of CAP, particularly those complicated by necrosis and empyema
[ 43,55 ]. In addition, these organisms occasionally cause pneumonia and frequently are seen
following influenza and chickenpox, respectively [ 44,45 ]. (See "Clinical features of varicella-
zoster virus infection: Chickenpox" and "Clinical features and diagnosis of seasonal influenza in
children", section on 'Pneumonia' .)
  The prevalence of M. pneumoniae and C. pneumoniae may be increasing in preschool children
with CAP [ 25,56 ]. (See "Pneumonia caused by Chlamydophila (Chlamydia) species in
children" and "Mycoplasma pneumoniae infection in children", section on 'Epidemiology' .)

In children ≥5 years

 S. pneumoniae is the most common typical bacterial cause of pneumonia in children older than
five years (see "Pneumococcal pneumonia in children", section on 'Epidemiology' )
 M. pneumoniae is more common among children ≥5 years than among younger children
(see "Mycoplasma pneumoniae infection in children", section on 'Epidemiology' )
 C. pneumoniae also is emerging as a frequent cause of pneumonia in older children and young
adults (see "Pneumonia caused by Chlamydophila (Chlamydia) species in children" )

Aspiration pneumonia — When there is a predisposition to aspiration, pneumonia may be caused by

anaerobic oral flora, including:

 Anaerobic streptococci (eg, Peptostreptococcus )

 Fusobacterium spp
 Bacteroides spp
 Prevotella melaninogenica

Risk factors for aspiration include a history of seizure, anesthesia, or other episode of reduced level of
consciousness, neurologic disease, dysphagia, gastroesophageal reflux, alcohol or substance abuse,
use of a nasogastric tube, or foreign body aspiration.

Nosocomial pneumonia — Nosocomial bacterial pneumonia is usually caused by gram-negative

bacilli or S. aureus . Nosocomial pneumonia frequently occurs in intensive care units where mechanical
ventilation, indwelling catheters, and administration of broad-spectrum antibiotics are common.
(See "Inpatient treatment of pneumonia in children", section on 'Nosocomial pneumonia' .)

In addition, during the winter respiratory viral season, all patients in a medical care environment are at
risk for nosocomial pneumonia caused by RSV, parainfluenza, and influenza viruses. (See "Clinical
features and diagnosis of seasonal influenza in children" and "Parainfluenza viruses in children", section
on 'Clinical presentation' and "Respiratory syncytial virus infection: Clinical features and diagnosis",
section on 'Transmission' .)

Special populations

Immunocompromised — The causes of pneumonia in immunocompromised hosts include all of the

pathogens mentioned above, as well as a variety of other organisms, as discussed below.

Gram-negative bacilli and S. aureus are common etiologies in neutropenic patients or in those with
white blood cell (WBC) defects. Clinically significant Legionellosis usually is seen only in
immunocompromised hosts with an exposure to an aquatic reservoir of Legionella pneumophila , such
as a river, lake, air-conditioning cooling tower, or water distribution systems [ 21,57 ]. However,
seroepidemiologic studies suggest that subclinical or minor infections occur in children [ 58,59 ].
(See "Epidemiology and pathogenesis of Legionella infection" .)

Opportunistic fungi, such as Aspergillus spp and Fusarium spp, also are a concern in neutropenic
patients and in those receiving immunosuppressive therapies that impair the cell-mediated response.
One of the more common pneumonia pathogens diagnosed in HIV-infected patients is Pneumocystis
jirovecii , which was formerly called Pneumocystis carinii [ 60 ]. (See "Epidemiology and clinical
manifestations of invasive aspergillosis" and "Mycology, pathogenesis, and epidemiology of Fusarium
infection" and "Natural history and classification of pediatric HIV infection", section on 'Pneumocystis
jirovecii pneumonia' .)

Viral causes of pneumonia, which may be life-threatening in the immunocompromised host, include:
  Rubeola (Hecht giant-cell pneumonia) (see "Clinical presentation and diagnosis of measles",
section on 'Immunocompromised patients' )
 Varicella-zoster virus (VZV) (see "Clinical features of varicella-zoster virus infection:
Chickenpox", section on 'Pneumonia' )
 CMV (see "Cytomegalovirus infection and disease in newborns, infants, children and
adolescents", section on 'CMV infections in immunocompromised hosts' )
 Epstein-Barr virus (EBV), which may be the trigger for lymphocytic interstitial pneumonitis, an
indolent but progressive process that occurs in children infected with HIV (see "Clinical
manifestations and treatment of Epstein-Barr virus infection" and "Lymphocytic interstitial
pneumonitis in children", section on 'Pathogenesis' )

Cystic fibrosis — Young children with cystic fibrosis frequently are infected with S. aureus , P.
aeruginosa , and H. influenzae (mostly nontypeable strains). Later in the course of the disease,
multiple drug-resistant gram-negative organisms, such as Burkholderia cepacia , Stenotrophomonas
maltophilia , andAchromobacter xylosoxidans , can be recovered. Aspergillus spp and nontuberculous
mycobacteria also may cause disease in this population. Cystic fibrosis lung disease is discussed in
detail separately. (See "Cystic fibrosis: Clinical manifestations of pulmonary disease" and "Cystic
fibrosis: Overview of the treatment of lung disease" and "Cystic fibrosis: Antibiotic therapy for lung
disease" .)

Sickle cell anemia — The prevalence of pneumonia is increased in children with sickle cell anemia
[ 61 ]. Atypical bacterial pathogens appear to be most frequent and are more commonly associated
with the acute chest syndrome. Other bacterial causes of pneumonia in children with sickle cell anemia
include S. pneumoniae , S. aureus , and H. influenzae [ 9 ]. (See "The acute chest syndrome in
children and adolescents with sickle cell disease", section on 'Infection' .)

Environmental considerations

Geography — Residence in or travel to specific geographic areas should suggest endemic pathogens:

 Tuberculosis is most common in immigrants from countries with a high prevalence of infection
(eg, countries throughout Asia, Africa, Latin America, and Eastern Europe) ( figure 2 ).
(See "Epidemiology of tuberculosis" .)
 Measles pneumonia is common in the developing world. (See "Clinical presentation and
diagnosis of measles" .)
 Coccidioides immitis is endemic to the southwestern United States, northern Mexico, and parts
of Central and South America. (See "Primary coccidioidal infection" .)
 Blastomyces dermatitidis , causing blastomycosis, is endemic in the southeastern and central
states and the midwestern states bordering the Great Lakes. (See "Mycology, pathogenesis,
and epidemiology of blastomycosis" and "Treatment of blastomycosis" .)
 Histoplasma capsulatum is in the Ohio, Missouri, and Mississippi river valleys in the United
States. It also occurs in Canada, Central America, eastern and southern Europe, parts of Africa,
eastern Asia, and Australia. Activities potentially leading to exposure to bird droppings and bat
guano may be suggestive. These include gardening, construction, cleaning of barns and
outbuildings, and spelunking. (See "Pathogenesis and clinical features of pulmonary
histoplasmosis" and "Diagnosis and treatment of pulmonary histoplasmosis" .)
 In the United States, hantavirus cardiopulmonary syndrome (acute febrile illness associated
with respiratory failure, shock, and high mortality) occurs predominantly west of the Mississippi
River (in the “four corners” region where the borders of Colorado, New Mexico, Arizona, and
Utah meet) after environmental exposure to infected deer mouse ( Peromyscus maniculatus )
saliva, urine, or feces. Activities associated with exposure include cleaning of barns and
outbuildings, trapping rodents, animal herding, and farming with hand tools.
(See "Epidemiology and diagnosis of hantavirus infections" and"Hantavirus cardiopulmonary
syndrome" .)

Animal exposures — Histoplasmosis is associated with exposure to bird droppings and bat guano,
and hantavirus infection is associated with exposure to an infected deer mouse. Other causes of
pneumonia that are associated with animal exposure include:

 Chlamydophila (formerly Chlamydia ) psittaci (psittacosis), which is transmitted to man

predominantly from birds (see "Psittacosis" )
  Coxiella burnetii (Q fever), which is associated with exposure to parturient sheep, goats, cattle,
and cats (or exposure to dust/soil contaminated by these animals) (see "Microbiology and
epidemiology of Q fever" and "Clinical manifestations and diagnosis of Q fever" )

Other exposures — Exposure to individuals at high risk for tuberculosis is a risk factor for the
development of tuberculosis in children. High-risk individuals include the homeless, recent immigrants
from endemic regions ( figure 2 ), incarcerated individuals, and HIV-infected patients.
(See "Epidemiology of tuberculosis".)

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 5 th to 6 th 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 10 th to 12 th 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 e-
mail 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 topics (see "Patient information: Pneumonia in children (The Basics)" )

SUMMARY — Pneumonia is more common in children younger than five years of age than in older
children and adolescents. Risk factors for pneumonia include environmental crowding, having school-
aged siblings, and underlying cardiopulmonary and other medical disorders.
(See 'Epidemiology' above.)

Pneumonia can be caused by a large number of microorganisms ( table 1A-B ). The agents commonly
responsible vary according to the age of the child and the setting in which the infection is acquired.
(See 'Etiologic agents' above.)

 In children younger than five years, viruses are most common. However, bacterial pathogens,
including S. pneumoniae , S. aureus , and S. pyogenes , also are important. (See 'In children
<5 years' above.)
 In otherwise-healthy children older than five years, S. pneumonia , M. pneumoniae ,
and Chlamydophila pneumoniae are most common. (See 'In children ≥5 years' above.)
 Community-associated methicillin-resistant S. aureus (CA-MRSA) is an increasingly important
pathogen in children of all ages, particularly in those with necrotizing pneumonia. S.
pneumoniae is another frequent cause of necrotizing pneumonia. (See 'Overview' above.)
 Aspiration pneumonia is usually caused by anaerobic oral flora. (See 'Aspiration
pneumonia' above.)
 Nosocomial pneumonia is usually caused by gram-negative bacilli or Staphylococcus aureus .
(See 'Nosocomial pneumonia' above.)

Clinical features and diagnosis of community-acquired pneumonia in

children
INTRODUCTION — Community-acquired pneumonia (CAP) is defined as signs and symptoms of an
acute infection of the pulmonary parenchyma in a previously healthy patient who acquired the infection
in the community, as distinguished from hospital-acquired (nosocomial) pneumonia [ 1,2 ]. CAP is a
common and potentially serious illness with considerable morbidity.

The clinical features and diagnosis of CAP in children will be reviewed here. The epidemiology,
pathogenesis, and treatment of pneumonia in children are discussed separately. (See "Epidemiology,
pathogenesis, and etiology of pneumonia in children" and "Outpatient treatment of community-
acquired pneumonia in children"and "Inpatient treatment of pneumonia in children" .)
CLINICAL PRESENTATION — The clinical presentation of childhood pneumonia varies depending
upon the responsible pathogen, the particular host, and the severity. The presenting signs and
symptoms are nonspecific; no single symptom or sign is pathognomonic for pneumonia in children.

Symptoms and signs of pneumonia may be subtle, particularly in infants and young children. The
combination of fever and cough is suggestive of pneumonia; other respiratory findings (eg, tachypnea,
increased work of breathing) may precede cough. Cough may not be a feature initially since the alveoli
have few cough receptors. Cough begins when the products of infection irritate cough receptors in the
airways. The longer fever, cough, and respiratory findings are present, the greater the likelihood of
pneumonia [ 3 ].

Neonates and young infants may present with difficulty feeding, restlessness, or fussiness [ 4 ]. Young
children (ie, <5 to 10 years of age) may present with fever and leukocytosis [ 3,5 ]. Older children
may complain of pleuritic chest pain (pain with respiration), but this is an inconsistent finding.
Occasionally, the predominant manifestation may be abdominal pain (because of referred pain from
the lower lobes) or nuchal rigidity (because of referred pain from the upper lobes). "Walking
pneumonia" is a term that is sometimes used to describe pneumonia in which the respiratory
symptoms do not interfere with normal activity.

CLINICAL EVALUATION — The evaluation of the child with cough and potential lower respiratory
tract disease has two goals: the identification of the clinical syndrome (eg, pneumonia, bronchiolitis,
asthma) and an assessment of the severity of the illness [ 4 ]. The severity of illness determines the
need for additional evaluation.

History — Important aspects of the history for children with possible community-acquire pneumonia
are listed in the table ( table 1 ) [ 4,6,7 ]. Historical features can be helpful in determining the etiologic
agent, the likelihood of infection with an organism that is resistant to antibiotics, and the severity of
illness. (See"Epidemiology, pathogenesis, and etiology of pneumonia in children", section on 'Etiologic
agents' .)

Examination — Important aspects of the examination are summarized in the table ( table 2 ) and
discussed in greater detail below.

General appearance — In the young infant, assessment of general appearance includes the ability to
attend to the environment, to feed, to vocalize, and to be consoled. The state of awareness and
presence of cyanosis should be assessed in all children, although children may be hypoxemic without
cyanosis [ 8 ]. Most children with radiographically confirmed pneumonia appear ill [ 9 ].

Fever — Fever is a common manifestation of pneumonia in children [ 10 ]. However, it is nonspecific

and variably present. Young infants may have afebrile pneumonia related to Chlamydia trachomatis or
other pathogens. (See "Chlamydia trachomatis infections in the newborn", section on
'Pneumonia' and"Epidemiology, pathogenesis, and etiology of pneumonia in children", section on 'In
infants' .)

Fever may be the only sign of occult pneumonia in highly febrile young children. In one report, 26
percent of 146 children (<5 years) with fever ≥39ºC, no clinical evidence of pneumonia or other
localizing signs, and peripheral white blood cell count ≥20,000/microL had radiographic evidence of
pneumonia [ 5 ].

Tachypnea — Tachypnea is the most sensitive and specific sign of radiographically confirmed
pneumonia in children [ 4,11-13 ]. In a systematic review of studies evaluating the correlation between
clinical examination findings and radiographic pneumonia, tachypnea was twice as frequent in children
with than without radiographic pneumonia, and the absence of tachypnea was the single most valuable
sign for excluding pneumonia [ 4 ]. Tachypnea in infants with pneumonia (respiratory rate
>70 breaths/min) also has been associated with hypoxemia [ 14 ]. Tachypnea may be less useful early
in the course of illness (eg, less than three days) [ 11 ].

The World Health Organization age-related definitions of tachypnea are as follows [ 15,16 ]:
  Younger than two months: >60 breaths/min
 Two to 12 months: >50 breaths/min
 One to 5 years: >40 breaths/min
 ≥5 years: >20 breaths/min

The respiratory rate varies with activity in infants and young children, and in these patients is best
assessed by counting for a full 60 seconds [ 4,17-19 ]. Observation of chest wall movements is
preferable to auscultation because auscultation may stimulate the child, falsely elevating the rate [ 4 ].
The respiratory rate may increase by as many as 10 breaths per minute per degree (Celsius) of fever
in children without pneumonia [ 20 ]; the effect of fever on respiratory rate in children with pneumonia
has not been investigated [ 4 ].

Respiratory distress — Signs of respiratory distress include tachypnea, hypoxemia (peripheral

arterial oxygen saturation [SpO 2 ] <90 percent on room air at sea level), increased work of breathing
(intercostal, subcostal, or suprasternal retractions; nasal flaring; grunting; use of accessory muscles),
apnea, and altered mental status [ 1 ].

Oxygen saturation should be measured in any child with increased work of breathing, particularly if he
or she has a decreased level of activity or agitation [ 1,2,21]. Infants and children with hypoxemia may
not appear cyanotic [ 8 ]. Hypoxemia is a sign of severe disease and an indication for admission
[ 1,2 ].

Signs of respiratory distress are more specific than fever or cough for lower respiratory tract infection.
In a review of 192 febrile infants younger than three months of age, the specificity of at least one sign
of respiratory distress for radiographic pneumonia (respiratory rate >60 breaths/min, retractions,
flaring, rales, grunting, apnea, or cyanosis) was 93 percent, but the sensitivity was only 59 percent
[ 22 ].

Signs of respiratory distress that are predictive of pneumonia include hypoxemia (defined differently in
different studies, usually oxygen saturation <94 to 96 percent in room air), retractions, head bobbing,
and nasal flaring [ 7,9,12,23 ]. Unlike tachypnea, the absence of these findings does not exclude a
diagnosis of pneumonia.

 In a review of children 2 to 59 months of age, oxygen saturation ≤96 percent in room air was
2.8 times more frequent among children with pneumonia than without [ 12 ]
 In a systematic review, retractions were 2.5 times more frequent in infants with pneumonia
than without [ 4 ]
 Nasal flaring is approximately three times more frequent in children <5 years with pneumonia
than without [ 4 ], and five times more frequent in infants 2 to 12 months with pneumonia than
without [ 12 ]
 Grunting, when present, is a sign of severe disease and impending respiratory failure [ 24 ]

Lung examination — Examination of the lungs may provide clues to the diagnosis of
pneumonia and/or potential complications.

Auscultation is an important component of the examination of the child who presents with findings
indicative of pneumonia. However, auscultatory findings have less interobserver agreement than
observable findings, such as retractions [ 4 ]. Auscultation of all lung fields should be performed.

Examination findings consistent with radiographically confirmed pneumonia include [ 13 ]:

 Crackles, also called rales or crepitations; in a systematic review, crackles were 3.5 times more
frequent in infants with radiographic pneumonia than without [ 4 ]
 Findings consistent with consolidated lung parenchyma, including:

 Decreased breath sounds

 Bronchial breath sounds (louder than normal, with short inspiratory and long expiratory phases,
and higher-pitched during expiration), egophony (E to A change)
 Bronchophony (the distinct transmission of sounds such as the syllables of “ninety-nine”)
 Whispered pectoriloquy (transmission of whispered syllables)
  Tactile fremitus (eg, when the patient says “ninety-nine”)
 Dullness to percussion

 Wheezing is more common in pneumonia caused by atypical bacteria and viruses [ 25 ] than
bacteria (see 'Clues to etiology' below)
 Findings suggestive of pleural effusion include chest pain with splinting, dullness to percussion,
distant breath sounds, and a pleural friction rub (see"Epidemiology; clinical presentation; and
evaluation of parapneumonic effusion and empyema in children", section on 'Clinical
presentation' )

Severity assessment — An assessment of pneumonia severity is necessary to determine the need

for laboratory and imaging studies and the appropriate treatment setting. The severity of pneumonia is
assessed by the child's overall clinical appearance and behavior, including an assessment of his or her
degree of awareness and willingness to eat or drink ( table 3 ) [ 7 ].

Clues to etiology — Clinical features classically taught to be characteristic of bacterial pneumonia,

atypical bacterial pneumonia, or viral pneumonia are summarized in the table ( table 4 ). However, the
features frequently overlap and cannot be used reliably to distinguish between the various etiologies
[ 26,27 ]. In addition, as many as 50 percent of infections may be mixed bacterial/viral infections.
(See "Epidemiology, pathogenesis, and etiology of pneumonia in children", section on 'Community-
acquired pneumonia' .)

 Bacterial – Classically, bacterial ("typical") pneumonia, usually resulting from Streptococcus

pneumoniae and less commonly from Staphylococcus aureusand group A streptococcus , which
may follow days of upper respiratory tract infection symptoms, is considered abrupt in onset,
with the febrile patient appearing ill and sometimes toxic. Respiratory distress is moderate to
severe; auscultatory findings may be few and focal, limited to the involved anatomic segment.
Signs and symptoms of sepsis and localized chest pain (signifying pleural irritation) are more
suggestive of bacterial etiology [ 10 ], as they are rarely present in nonbacterial pneumonia.
Complications, discussed below, also are more suggestive of bacterial etiology
(see 'Complications' below) On the other hand, primary bacterial pneumonia is unlikely in
children older than five years if wheezing is present [ 28 ].

Pneumococcal pneumonia is the most common typical bacterial pneumonia in children of all
ages. In one retrospective review of 254 children and young adults (age <1 month to 26 years)
with pneumococcal pneumonia, the most common signs and symptoms and their approximate
frequencies are listed below [ 29 ]:

 Fever: 90 percent
 Cough: 70 percent; productive cough: 10 percent
 Tachypnea: 50 percent
 Malaise/lethargy: 45 percent
 Emesis: 43 percent
 Hypoxemia (oxygen saturation ≤95 percent): 50 percent
 Decreased breath sounds: 55 percent
 Crackles: 40 percent

Pneumococcal pneumonia in children is discussed in greater detail separately. (See "Pneumococcal

pneumonia in children" .)

 Atypical bacterial – "Atypical" bacterial pneumonia resulting from Mycoplasma

pneumoniae or Chlamydophila (formerly Chlamydia ) pneumoniae usually presents abruptly
with constitutional findings of fever, malaise and myalgia, headache, photophobia, sore throat,
and gradually worsening nonproductive cough despite improvement of other symptoms
[ 25,28 ]. Although hoarseness may be seen in disease caused by both agents, it is more
frequently seen with C. pneumoniae infection. Wheezing is a frequent finding in atypical
bacterial and viral pneumonias [ 10 ]. (See "Pneumonia caused by Chlamydophila (Chlamydia)
species in children" and "Mycoplasma pneumoniae infection in children", section on 'Clinical
features' .)
 M. pneumoniae may be associated with a variety of extrapulmonary manifestations.
Dermatologic manifestations may range from a mild erythematous maculopapular rash or
urticaria to the Stevens-Johnson syndrome. Other extrapulmonary manifestations include
hemolytic anemia, polyarthritis, pancreatitis, hepatitis, pericarditis, myocarditis, and neurologic
complications [ 30 ]. (See "Mycoplasma pneumoniae infection in children", section on 'Clinical
features' .)

Infants younger than one year of age may develop "afebrile pneumonia of infancy". Afebrile
pneumonia of infancy is a syndrome generally seen between two weeks and three to four
months of life. It is classically caused by C. trachomatis , but other agents, such as
cytomegalovirus, M. hominis , and Ureaplasma urealyticum , also are implicated. The clinical
presentation is one of insidious onset of rhinorrhea and tachypnea followed by a staccato cough
pattern (individual coughs separated by inspirations). Physical examination typically reveals
diffuse inspiratory crackles. Conjunctivitis may be present, or there may have been a past
history of conjunctivitis [ 31 ]. (See "Chlamydia trachomatis infections in the newborn", section
on 'Pneumonia' .)
 Viral – The onset of viral pneumonia is gradual and associated with preceding upper airway
symptoms (eg, rhinorrhea, congestion). The child does not appear toxic. Auscultatory findings
are usually diffuse and bilateral. In one study of 98 ambulatory children with pneumonia,
wheezing was more frequent in patients with viral than bacterial pneumonia (43 versus 16
percent), but other clinical features often associated with viral illness, such as rhinorrhea,
myalgia, and ill contacts, were not [ 32 ].

Some viral causes of pneumonia are associated with characteristic dermatologic findings:

 Measles ( picture 1A-B ) (see "Clinical presentation and diagnosis of measles" )

 Varicella ( picture 2 ) (see "Clinical features of varicella-zoster virus infection: Chickenpox" )
 Herpes simplex virus ( picture 3A-B ) (see "Clinical manifestations and diagnosis of herpes
simplex virus type 1 infection", section on 'Respiratory tract infections' and "Neonatal herpes
simplex virus infection: Clinical features and diagnosis", section on 'Disseminated disease' )

RADIOLOGIC EVALUATION — The presence of an infiltrate on chest radiograph is often used to

define pneumonia, particularly in clinical research [ 23,33 ]. The radiographic definition is necessary
because of the difficulty in obtaining appropriate specimens from the lower respiratory tract for culture
or microbiologic evaluation. This peculiarity makes it difficult to assess the degree to which chest
radiographs are actually needed to diagnose pneumonia in the clinical setting, as the likelihood ratio of
a standard cannot be measured [ 4,7 ].

Indications — Routine chest radiographs are not necessary to confirm the diagnosis of suspected
community-acquired pneumonia (CAP) in children with mild, uncomplicated lower respiratory tract
infection who are well enough to be treated as outpatients [ 1,2,7 ]. Indications for radiographs in
children with clinical evidence of pneumonia include [ 1,2,7 ]:

 Severe disease ( table 3 ) (see 'Severity assessment' above)

 Confirmation of the diagnosis when clinical findings are inconclusive
 Hospitalization (to document the presence, size, and character of parenchymal infiltrates and
evaluate potential complications)
 Exclusion of alternate explanations for respiratory distress (eg, foreign body aspiration, heart
failure), particularly in patients with underlying cardiopulmonary or medical conditions
(see 'Differential diagnosis' below)
 Assessment of complications, particularly in children whose pneumonia is prolonged and
unresponsive to antimicrobial therapy [ 7 ] (see "Outpatient treatment of community-acquired
pneumonia in children", section on 'Treatment failure' and 'Complications' below)
 Exclusion of pneumonia in young children (3 to 36 months) with fever >39ºC and leukocytosis
(≥20,000 white blood cell [WBC]/microL) and older children (<10 years) with fever >38ºC,
cough, and leukocytosis (≥15,000 WBC/microL) [ 3,5 ] (see "Fever without a source in children
3 to 36 months of age" )

There are a number of caveats to consider when deciding whether to obtain radiographs and whether
radiographs will alter management. These include:
  Radiographic findings are poor indicators of the etiologic diagnosis and must be used in
conjunction with other clinical features to make therapeutic decisions [ 2,34-37 ]
(see "Outpatient treatment of community-acquired pneumonia in children", section on
'Treatment failure' )
 Radiographic findings may lag behind the clinical findings [ 38 ]
 Patients who are hypovolemic may have normal-appearing chest radiography before volume
repletion
 There is variation in intraobserver and interobserver agreement [ 2,39 ]
 Radiographic interpretation may be influenced by the clinical information that is provided to the
radiologist [ 40 ]
 Obtaining outpatient chest radiographs does not affect outcome [ 41 ]

Views — When radiographs are indicated, the recommended views depend upon the age of the child
[ 42 ]. In children older than four years, the frontal posteroanterior (PA) upright chest view is usually
obtained to minimize the cardiac shadow [ 43 ]. In younger children, position does not affect the size
of the cardiothoracic shadow, and the anteroposterior (AP) supine view is preferred because
immobilization is easier and the likelihood of a better inspiration is improved [ 43 ].

There is a lack of consensus regarding the need for lateral radiographs to demonstrate infiltrates
behind the dome of the diaphragm or the cardiac shadow that may not be visualized on AP or PA views
[ 44 ]. In a review of chest radiographs in 201 children with pneumonia, the lateral film was abnormal
in 91 percent of 109 children with definite pneumonia [ 45 ]. However, it was the sole basis for the
diagnosis in only three cases.

We suggest that a lateral view be obtained in settings where the radiographs are interpreted by
nonradiologists. The Pediatric Infectious Diseases Society and Infectious Diseases Society of America
suggest PA and lateral views for all children who are hospitalized for management of CAP [ 1 ]. The
British Thoracic Society guidelines recommend against lateral radiographs [ 2 ].

A lateral decubitus radiograph (with the affected side down) may be needed to identify the presence of
a pleural effusion. (See "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion
and empyema in children", section on 'Radiologic evaluation' .)

High-resolution computed tomography and ultrasonography are available for patients who require
more extensive imaging or clarification of plain radiographic findings [ 46 ].

Etiologic clues — Certain radiographic features that are more often associated with bacterial,
atypical bacterial, or viral etiologies are listed below. However, none can reliably differentiate between
a bacterial, atypical bacterial, and viral pneumonia ( table 4 ) [ 26,47-49 ].

 Segmental consolidation is reasonably specific for bacterial pneumonia but lacks sensitivity
[ 36,50 ]. Radiologic features of segmental consolidation are not always easy to distinguish
from segmental collapse (atelectasis), which is apparent in about 25 percent of children with
bronchiolitis [ 51,52 ].
 In clinical practice it is common to consider alveolar infiltrates to be caused by bacteria and
bilateral diffuse interstitial infiltrates to be caused by atypical bacterial or viral infections.
However, this is not supported in the literature. In a study of 254 children with radiographically
defined pneumonia, the etiology was determined in 215 [ 35 ]. The sensitivity and specificity of
alveolar infiltrate for bacterial pneumonia were 72 and 51 percent, respectively; the sensitivity
and specificity of interstitial infiltrates for viral pneumonia were 49 and 72 percent, respectively.
A lobar infiltrate is reasonably specific for a bacterial pneumonia but lacks sensitivity [ 29,53 ].
 Pulmonary consolidation in young children sometimes appears to be spherical (ie, "round
pneumonia") [ 54,55 ]. Round pneumonias tend to be >3 cm, solitary, and posteriorly located
[ 55,56 ]. The most common bacterial etiology for round pneumonia is S. pneumoniae ;
additional bacterial causes include other streptococci, Haemophilus influenzae , S. aureus ,
and M. pneumoniae [ 36,57 ].
 Pneumatoceles, cavitations, large pleural effusions ( image 1A-B ), and necrotizing processes
( image 2 ) are supportive of a bacterial etiology.
 M. pneumoniae and viruses are most likely to spread diffusely along the branches of the
bronchial tree, resulting in a bronchopneumonic pattern ( image 3 ). However, S.
 pneumoniae have been associated with a similar radiographic pattern in children.
(See "Pneumococcal pneumonia in children", section on 'Radiographic features' .)
 In young infants, hyperinflation with an interstitial process is characteristic of afebrile
pneumonia of infancy, typically caused by C. trachomatis . (See"Chlamydia trachomatis
infections in the newborn", section on 'Pneumonia' .)
 Significant mediastinal/hilar adenopathy suggests a mycobacterial or fungal etiology.

LABORATORY EVALUATION — The laboratory evaluation of the child with community-acquired

pneumonia (CAP) depends on the clinical scenario, including the age of the child, severity of illness,
presence of potential complications, and whether the child requires hospitalization [ 1 ]. More
aggressive evaluation is required when it is necessary to determine a microbiologic etiology (eg, in
children with severe disease, potential complications, and who require hospital admission) [ 2 ]. An
etiologic diagnosis in such children helps to direct pathogen-specific therapy and permits cohorting of
children if necessary to prevent the spread of nosocomial infection.

Young infants in whom pneumonia is suspected, particularly those who are febrile and toxic appearing,
require a full evaluation for sepsis and other serious bacterial infections. (See "Evaluation and
management of fever in the neonate and young infant (less than three months of age)" .)

Blood tests — Complete blood count (CBC) with differential and acute phase reactants may provide
supportive evidence for bacterial or viral pneumonia, but should not be used as the only criteria in
determining the need for antimicrobial therapy. Serum electrolytes may be useful in assessing the
degree of dehydration and the presence of hyponatremia, which may indicate the syndrome of
inappropriate antidiuretic hormone secretion (SIADH). (See "Pathophysiology and etiology of the
syndrome of inappropriate antidiuretic hormone secretion (SIADH)", section on 'Pulmonary disease' .)

 Complete blood count – CBC usually is not necessary for children with mild lower respiratory
tract infection who will be treated as outpatients, unless the CBC will determine the need for
antibiotic therapy. CBC typically is performed in infants and children who require hospital
admission. Certain CBC findings, described below, are more characteristic of bacterial, atypical
bacterial, or viral pneumonias. However, the findings overlap and cannot reliably differentiate
between the etiologic agents.

 White blood cell (WBC) count <15,000/microL suggests a nonbacterial etiology, except in the
severely ill patient, who also may be neutropenic and have a predominance of immature cells.
 WBC count >15,000/microL is suggestive of pyogenic bacterial disease [ 58 ]. However,
children with M. pneumoniae , influenza, or adenovirus pneumonia also may have WBC
count >15,000/microL [ 59-61 ].
 Peripheral eosinophilia may be present in infants with afebrile pneumonia of infancy, typically
caused by C. trachomatis . (See "Chlamydia trachomatis infections in the newborn", section on
'Pneumonia' .)

 Acute phase reactants – Acute phase reactants, such as the erythrocyte sedimentation rate, C-
reactive protein (CRP), and serum procalcitonin (PCT), need not be routinely measured in fully
immunized children with CAP managed as outpatients [ 1 ]. However, for those with more
serious disease requiring hospitalization, measurement of acute phase reactants may provide
useful information to assist clinical management.

Measurement of serum CRP may be helpful in distinguishing bacterial from viral pneumonia. A
meta-analysis of eight studies including 1230 patients suggested that children with bacterial
pneumonia were more likely to have serum CRP concentrations greater than 35 to 60 mg/L (3.5
to 6 mg/dL) than children with nonbacterial pneumonia (odds ratio 2.6, 95% CI 1.2-5.6) [ 62 ].
Given a 41 percent prevalence of bacterial pneumonia, the positive predictive value for CRP
values of 40 to 60 mg/L (4 to 6 mg/dL) was 64 percent. An elevated serum PCT concentration
may be as sensitive as but more specific than an increased CRP level for differentiating a
bacterial from a viral process [ 26,63,64 ]. However, predictable utility has not been
documented [ 1,65,66 ].

Acute phase reactants should not be used as the sole determinant to distinguish between viral
and bacterial etiologies of CAP but may be helpful in following the disease course, response to
 therapy, and in determining when therapy can be discontinued [ 1,65,67,68 ]. (See "Inpatient
treatment of pneumonia in children", section on 'Duration of treatment' .)
 Serum electrolytes – Measurement of serum electrolytes may be helpful in assessing the degree
of dehydration in children with limited fluid intake and whether hyponatremia is present (as
pneumonia may be complicated by SIADH). (See 'Complications' below.)

Microbiology

Indications — If possible, a microbiologic diagnosis should be established in children with severe

disease ( table 3 ), potential complications, and those who require hospitalization. Accurate and rapid
diagnosis of the responsible pathogen helps to determine the appropriate antimicrobial therapy [ 1 ].
(See "Inpatient treatment of pneumonia in children", section on 'Overview' .)

A microbiologic diagnosis also should be established if there appears to be a community outbreak

[ 69 ] or if an unusual pathogen is suspected, particularly if it requires treatment that differs from
standard empiric regimens (eg, S . aureus including methicillin-resistant strains, Mycobacterium
tuberculosis ). (See 'Critical microbes' below.)

Children with mild disease who are treated as outpatients usually can be treated empirically, based on
age and other epidemiologic features, without establishing a microbiologic etiology [ 2,70 ].
(See "Outpatient treatment of community-acquired pneumonia in children", section on 'Empiric
therapy' .)

Microbiologic diagnosis can be established with culture, rapid diagnostic testing (enzyme immunoassay,
immunofluorescence, polymerase chain reaction [PCR]), or serology.

Cultures

 Blood cultures – We suggest that blood cultures be performed in children with CAP who require
admission to the hospital and in children with parapneumonic effusion or other complication
[ 1,2,71 ]. Although blood cultures are positive in at most 10 to 12 percent of children with
pneumonia, when positive they help to confirm the etiologic diagnosis [ 72-74 ]. The yield of
blood cultures increases to 30 to 40 percent in patients with a parapneumonic effusion or
empyema [ 74-76 ]. The utility of blood culture is limited when antibiotics are administered
before obtaining the specimen. (See "Blood cultures for the detection of bacteremia" .)

Blood cultures are not necessary in children with CAP who will be treated as outpatients
[ 1,7,72,77 ]. In the outpatient setting, the likelihood of a positive blood culture in children with
CAP is less than 3 percent [ 72,73 ].
 Nasopharyngeal cultures – We do not suggest obtaining nasopharyngeal (NP) cultures for
etiologic diagnosis in children with pneumonia. Bacterial organisms recovered from the
nasopharynx do not accurately predict the etiology of pneumonia because bacteria that cause
pneumonia also may be normal upper respiratory flora. The results of NP cultures for viruses
and atypical bacterial although helpful may not be available soon enough to assist with
management decisions [ 7 ]. Rapid diagnostic tests for viruses and atypical bacteria are
discussed below. (See 'Rapid diagnostic tests' below.)
 Sputum cultures – We suggest that sputum samples for Gram stain and culture be obtained in
children who require hospital admission if they are able to produce sputum [ 1 ]. Children
younger than five years usually swallow sputum, so it is rarely available for examination. Good-
quality sputum samples can be obtained by sputum induction [ 78 ]. However, sputum
induction is unpleasant and not routinely necessary because most children respond to empiric
antimicrobial therapy. It may be beneficial in children who require intensive-care therapy, have
a pleural effusion, or fail to respond to empiric therapy [78,79 ]. (See "Inpatient treatment of
pneumonia in children", section on 'Empiric therapy' .)

As a general guide, an appropriate sputum specimen for examination is one with ≤10 epithelial
cells and ≥25 polymorphonuclear leukocytes (PMN) under low power (x100) [ 80 ]. A
predominant microorganism and/or intracellular organisms suggest the etiologic agent. When
the following criteria are used, the specificity of the Gram stain for identifying pneumococci has
been shown to be 85 percent, with a sensitivity of 62 percent: predominant flora or more than
10 Gram-positive, lancet-shaped diplococci per oil immersion field (x1000) ( picture 4 ) [ 81 ].
  Pleural fluid cultures – Diagnostic (and possibly therapeutic) thoracentesis generally is
warranted for children with more than minimal pleural effusion. Specimens for culture of pleural
fluid ideally should be obtained before administration of antibiotics. The evaluation of pleural
fluid is discussed separately. (See "Epidemiology; clinical presentation; and evaluation of
parapneumonic effusion and empyema in children", section on 'Pleural fluid analysis' .)

Rapid diagnostic tests — Rapid diagnostic tests, such as molecular testing using PCR techniques
and immunofluorescence, on NP specimens can be helpful in the management of infants and children
who are admitted to the hospital with probable viral or atypical bacterial CAP. The results of rapid
diagnostic tests can be used to make decisions about treatment and cohorting of patients [ 1 ]. The
rapid diagnostic tests that are available for the following pathogens are discussed separately:

 Respiratory syncytial virus (see "Respiratory syncytial virus infection: Clinical features and
diagnosis", section on 'Diagnosis' )
 Influenza viruses (see "Clinical features and diagnosis of seasonal influenza in children", section
on 'Diagnosis' )
 Parainfluenza viruses (see "Parainfluenza viruses in children", section on 'Diagnosis' )
 Adenovirus (see "Diagnosis and treatment of adenovirus infection", section on 'Pneumonia' )
 M. pneumoniae (see "Mycoplasma pneumoniae infection in children", section on 'Diagnosis' )
 Chlamydophila spp (see "Pneumonia caused by Chlamydophila (Chlamydia) species in children",
section on 'Diagnosis' )
 Human metapneumovirus (see "Human metapneumovirus infections", section on 'Diagnosis' )

Serology — We do not suggest routine serologic testing for specific pathogens (eg, S.
pneumoniae , M. pneumoniae , C. pneumoniae ) because the results usually do not influence
management [ 7,82,83 ]. Serologic diagnosis of viral pathogens is not practical because acute and
convalescent specimens are needed. S. pneumoniae has too many potential infecting serotypes to
make antibody determinations practical. Serologic tests for Chlamydophila spp are not readily
available.

Although most older children with atypical pneumonia can be treated empirically for M. pneumoniae ,
serologic and PCR testing can be helpful in evaluating the younger child. These tests also may be
helpful in establishing the diagnosis of M. pneumoniae in patients with extrapulmonary manifestations,
particularly central nervous system manifestations. (See "Mycoplasma pneumoniae infection in
children", section on 'Clinical features' .)

Other tests — Other tests that may be helpful in establishing less common microbiologic etiologies of
CAP in children include:

 Tuberculin skin and interferon gamma release assay if pulmonary tuberculosis is a

consideration; additional diagnostic testing for tuberculosis in children is discussed separately
(see "Tuberculosis disease in children", section on 'Diagnosis' )
 Urine antigen testing for legionellosis due to serogroup 1 (see "Clinical manifestations and
diagnosis of Legionella infection", section on 'Urinary antigen testing' )
 Serum and urine antigen testing for histoplasmosis (see "Diagnosis and treatment of pulmonary
histoplasmosis", section on 'Antigen detection' )
 Urine antigen testing for S. pneumoniae in children should not be performed because of false
positive reactions, some of which may merely indicate colonization with S. pneumoniae [ 1,2 ]

Invasive studies — Invasive procedures may be necessary to obtain lower respiratory tract
specimens for culture and other studies in children in whom an etiologic diagnosis is necessary and has
not been established by other means [ 1,84-87 ]. These procedures are typically reserved for seriously
ill patients whose condition is worsening despite empiric therapy, or individuals with significant
comorbidities (eg, immune compromise). They include [ 1,84-86 ]:

 Bronchoscopy with bronchoalveolar lavage (BAL). Because the accurate identification of

bacterial pathogens via bronchoscopy is hampered by specimen contamination with upper
airway normal flora, quantitative culture techniques are utilized in many centers to differentiate
true infection from upper airway contamination [ 88-90 ].
  Percutaneous needle aspiration of the affected lung tissue guided by computed tomography or
ultrasonography. A small study from Finland found that needle aspiration determined an
infectious etiology (21 bacteria and 2 viruses) in 20 of 34 patients (59 percent) studied and in
18 of 26 (69 percent) of those in whom an adequate specimen was obtained [ 84 ]. Six patients
developed a pneumothorax, which spontaneously resolved over two to three days without
intervention.
 Lung biopsy either by a thoracoscopic or thoracotomy approach. Open biopsy yields diagnostic
information that may affect medical management in up to 90 percent of patients [ 86 ]. In one
retrospective review, an infectious etiology was determined by open lung biopsy in 10 of 33
patients with respiratory failure, eight of whom had a prior nondiagnostic BAL [ 85 ]. In another
retrospective review, lung biopsy provided a definitive diagnosis in 25 of 50
immunocompromised patients, nine of whom had a prior nondiagnostic BAL [ 91 ].

Critical microbes — Some microbes are critical to detect because they require treatment that differs
from standard empiric regimens or have public health implications. Diagnostic testing for these
pathogens is discussed separately.

 Influenza A and B (see "Clinical features and diagnosis of seasonal influenza in children",
section on 'Diagnosis' )
 Community-associated methicillin-resistant S. aureus (see "Treatment of invasive methicillin-
resistant Staphylococcus aureus infection in children", section on
'Pneumonia' and "Epidemiology and clinical spectrum of methicillin-resistant Staphylococcus
aureus infections in children", section on 'Epidemiology and risk factors' )
 M. tuberculosis (see "Tuberculosis disease in children" )
 Fungal etiologies ( Coccidioides immitis , Blastomyces dermatitidis , Histoplasma capsulatum )
(see "Primary coccidioidal infection" and "Mycology, pathogenesis, and epidemiology of
blastomycosis" and "Treatment of blastomycosis" and "Diagnosis and treatment of pulmonary
histoplasmosis" )
 Legionella species (see "Clinical manifestations and diagnosis of Legionella infection", section on
'Specific laboratory diagnosis' )
 Avian influenza (see "Clinical manifestations and diagnosis of avian influenza", section on
'Diagnosis' )
 Hantavirus (see "Hantavirus cardiopulmonary syndrome" )
 Agents of bioterrorism (see "Identifying and managing casualties of biological terrorism" )

DIAGNOSIS — The diagnosis of pneumonia requires historical or physical examination evidence of an

acute infectious process with signs or symptoms of respiratory distress or radiologic evidence of an
acute pulmonary infiltrate [ 7,30 ].

The diagnostic approach depends, to some extent, upon the setting and the severity of illness. In the
appropriate clinical setting, the diagnosis can be made without radiographs. In children with severe
illness, and in those who require hospital admission, the diagnosis should be confirmed with
radiographs. If possible, etiologic diagnosis should be established in children who require admission to
the hospital and in those who fail to respond to initial therapy. (See "Inpatient treatment of pneumonia
in children", section on 'Overview' .)

Clinical diagnosis — The diagnosis of pneumonia should be considered in infants and children with
respiratory complaints, particularly cough, tachypnea, retractions, and abnormal lung examination
[ 2,3,7 ].

The diagnosis of pneumonia can be made clinically in children with fever and historical or physical
examination evidence of an infectious process with symptoms or signs of respiratory distress [ 7 ].
Tachypnea, nasal flaring, grunting, retractions, rales, and decreased breath sounds increase the
likelihood of pneumonia [4,9,30,92 ]. The absence of tachypnea is helpful in excluding pneumonia; the
absence of the other signs is not. (See 'Tachypnea' above.)

In developing countries where there is a high prevalence of pneumonia, the presence of a single
positive respiratory sign increases the certainty of pneumonia [ 4]. The World Health Organization uses
tachypnea (>60 breaths/min in infants <2 months; >50 breaths/min in infants 2 to 12 months; and
>40 breaths/min in children 1 to 5 years; and >20 breaths/min in children ≥5 years) as the sole
criterion to define pneumonia in children with cough or difficulty breathing [ 15 ]. In developed
countries with a lower prevalence of pneumonia, multiple respiratory signs are necessary to increase
the certainty of pneumonia [ 4,93 ].

Radiographic confirmation — The presence of infiltrates on chest radiograph confirms the diagnosis
of pneumonia in children with compatible clinical findings. Radiographs should be obtained in children
in whom the diagnosis is uncertain and in those with severe, complicated, or recurrent pneumonia
[ 1,2,94 ]. Radiographic confirmation is not necessary in children with mild, uncomplicated lower
respiratory tract infection who will be treated as outpatients. (See'Indications' above.)

Radiographic findings cannot reliably distinguish between bacterial, atypical bacterial, and viral
etiologies of pneumonia. Radiographic findings should be used in conjunction with clinical and
microbiologic data to make therapeutic decisions [ 2,4 ]. (See "Outpatient treatment of community-
acquired pneumonia in children", section on 'Empiric therapy' and "Inpatient treatment of pneumonia
in children", section on 'Empiric therapy' .)

Etiologic diagnosis — The etiologic agent is suggested by host characteristics, clinical presentation,
epidemiologic considerations, and, to some degree, the results of nonspecific laboratory tests and
chest radiographic patterns ( table 4 ). (See 'Clues to etiology' above and 'Etiologic clues' above
and "Epidemiology, pathogenesis, and etiology of pneumonia in children", section on 'Etiologic
agents' .)

Specific microbiologic tests can be used to confirm the etiologic diagnosis. Confirmation of etiologic
diagnosis is not necessary in mildly ill patients who can be treated empirically in the outpatient setting.
Confirmation of etiologic diagnosis should be attempted in children who are admitted to the hospital or
are suspected to be infected with an unusual pathogen, or a pathogen that requires treatment that
differs from standard empiric regimens, so that therapy can be directed toward the appropriate
pathogen. Etiologic diagnosis also is necessary in children who fail to respond to initial therapy.
(See 'Microbiology' above and 'Critical microbes' above and "Inpatient treatment of pneumonia in
children", section on 'Empiric therapy' .)

DIFFERENTIAL DIAGNOSIS — Although pneumonia is highly probable in a child with fever,

tachypnea, cough, and infiltrate(s) on chest radiograph, alternate diagnoses and coincident conditions
must be considered in children who fail to respond to therapy or have an
unusual presentation/course [ 7 ].

The Table lists a number of other conditions that can mimic an infectious pneumonia ( table 5 ).
History and/or associated clinical features usually help to distinguish the conditions in the table from
infectious pneumonia. In some cases, laboratory studies or additional imaging may be necessary.

Foreign body aspiration must be considered in young children. The aspiration event may not have been
witnessed. (See "Airway foreign bodies in children", section on 'Presentation' .)

Other causes of tachypnea, with or without fever and cough, in infants and young children include
[ 95 ]:

 Bronchiolitis (see "Bronchiolitis in infants and children: Clinical features and diagnosis", section
on 'Clinical features' )
 Heart failure
 Sepsis
 Metabolic acidosis (see "Approach to the child with metabolic acidosis", section on 'Clinical
evaluation and diagnosis' )

These conditions usually can be distinguished from pneumonia by history, examination, and laboratory
tests.

Lemierre syndrome (jugular vein suppurative thrombophlebitis) is an important consideration in

adolescents and young adults whose illness began with pharyngitis. In Lemierre syndrome, the vessels
of the carotid sheath become infected (typically with Fusobacterium spp), leading to bacteremia and
metastatic spread of infection to the lungs and mediastinum. (See "Suppurative (septic)
thrombophlebitis", section on 'Jugular vein' .)

Community-acquired pneumonia (CAP) can be misdiagnosed in young children with asthma who have
viral respiratory infections [ 96 ]. Many such children have respiratory distress and may have
hypoxemia. The diagnosis of CAP and treatment with antibiotics must be carefully considered in young
children who have a prodrome compatible with a viral respiratory infection and wheezing, even if there
are pulmonary infiltrates (versus atelectasis) on chest radiograph. (See "Chronic asthma in children
younger than 12 years: Evaluation and diagnosis", section on 'Viral URI' .)

Rare, noninfectious lung diseases may present with an intercurrent infectious illness. Pulmonary
alveolar proteinosis, eosinophilic pneumonia, acute interstitial pneumonitis, and cryptogenic organizing
pneumonia are entities that should be considered, especially if the acute illness is atypical or the
radiographic and clinical findings do not resolve as expected with uncomplicated CAP. (See "Clinical
manifestations and etiology of pulmonary alveolar proteinosis in adults" and "Idiopathic acute
eosinophilic pneumonia" and "Acute interstitial pneumonia (Hamman-Rich
syndrome)" and "Cryptogenic organizing pneumonia" .)

COMPLICATIONS — Bacterial pneumonias are more likely than atypical bacterial or viral pneumonias
to be associated with complications involving the respiratory tract. Complications of bacterial
pneumonia include pleural effusion ( image 1A-B ), empyema, pneumatoceles, necrotizing pneumonia
( image 2 ), and lung abscesses.

Pleural effusion and empyema — The clinical features, evaluation, and management of
parapneumonic effusion and empyema in children are discussed separately. Hypoalbuminemia is
common in children with parapneumonic effusions and hypogammaglobulinemia may be encountered.
(See 'Blood tests' above and"Epidemiology; clinical presentation; and evaluation of parapneumonic
effusion and empyema in children" and "Management and prognosis of parapneumonic effusion and
empyema in children" .)

Necrotizing pneumonia — Necrotizing pneumonia, necrosis, and liquefaction of lung parenchyma, is

a serious complication of community-acquired pneumonia (CAP). Necrotizing pneumonia usually follows
pneumonia caused by particularly virulent bacteria [ 94 ]. S. pneumoniae (especially serotype 3 and
serogroup 19) is the most common cause of necrotizing pneumonia ( image 2 ) [ 97-102 ]. Necrotizing
pneumonia also may occur with S. aureus and group A streptococcus and has been reported due to M.
pneumoniae , Legionella , and Aspergillus . [ 102-106 ].

Clinical manifestations of necrotizing pneumonia are similar to those of uncomplicated pneumonia, but
they are more severe [ 107,108 ]. Necrotizing pneumonia should be considered in a child with
prolonged fever or septic appearance [ 94 ]. The diagnosis can be confirmed by chest radiograph
(which demonstrates a radiolucent lesion) ( image 4 ) or contrast-enhanced computed tomography
[ 109 ]; the findings on chest radiograph may lag behind those of computed tomography [ 105 ].

Pleural effusion/empyema generally accompanies necrotizing pneumonia whereas bronchopleural

fistula, pneumatocele, or abscess formation (which typically is insidious) is much less common.
Drainage of the pleural fluid collection is frequently required but pneumonectomy is rarely needed.
(See 'Pneumatocele' below and'Lung abscess' below.)

Treatment of necrotizing pneumonia is discussed separately. (See "Inpatient treatment of pneumonia

in children", section on 'Complicated CAP' .)

Lung abscess — A lung abscess is an accumulation of inflammatory cells, accompanied by tissue

destruction or necrosis that produces one or more cavities in the lung [ 44 ]. Aspiration is the most
important predisposing factor for lung abscess, which may develop one to two weeks after the
aspiration event; other predisposing factors include airway obstruction and congenitally abnormal lung
[ 44 ]. S. aureus is the organism most frequently involved [ 95 ].
Clinical manifestations of lung abscess are nonspecific and similar to those of pneumonia [ 44 ]. They
include fever, cough, dyspnea, chest pain, anorexia, hemoptysis, and putrid breath [ 44,94,110-112 ].
The course may be indolent.

The diagnosis is suggested by a chest radiograph demonstrating a thick-walled cavity with an air-fluid
level ( image 4 ) [ 44 ], and confirmed by contrast-enhanced computed tomography [ 109 ]. Lung
abscess is often accompanied by parapneumonic effusion [ 113,114 ]. Lung abscess should be
suspected when consolidation is unusually persistent, when pneumonia remains persistently round or
mass-like, and when the volume of the involved lobe is increased (as suggested by a bulging fissure)
[ 44,115 ].

Interventional radiology may be helpful in obtaining a specimen from the abscess cavity for diagnostic
studies. Treatment of lung abscess is discussed separately. (See "Inpatient treatment of pneumonia in
children", section on 'Complicated CAP' .)

The most common complication of lung abscess is intracavitary hemorrhage. This can cause
hemoptysis or spillage of the abscess contents with spread of infection to other areas of the lung
[ 107 ]. Other complications of lung abscess include empyema, bronchopleural fistula, septicemia,
cerebral abscess, and inappropriate secretion of antidiuretic hormone [ 107 ].

Pneumatocele — Pneumatoceles are thin-walled, air-containing cysts of the lungs. They are
classically associated with S. aureus , but may occur with a variety of organisms [ 116,117 ].
Pneumatoceles frequently occur in association with empyema [ 116 ]. In most cases, pneumatoceles
involute spontaneously, and long-term lung function is normal [ 116,118,119 ]. However, on occasion,
pneumatoceles result in pneumothorax [ 117 ].

Hyponatremia — Hyponatremia (serum sodium concentration ≤135 meq/L) occurs in approximately

45 percent of children with CAP and one-third of children hospitalized with CAP, but is usually mild
[ 120-122 ]. Inappropriate secretion of antidiuretic hormone (ADH) is the most frequent cause
[ 120,121 ]. Hyponatremia is associated with increased length of hospital stay, complications, and
mortality. (See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone
secretion (SIADH)", section on 'Pulmonary disease' .)

INDICATIONS FOR HOSPITALIZATION — Indications for hospitalization are discussed separately.

(See "Inpatient treatment of pneumonia in children", section on 'Indications' .)

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 5 th to 6 th 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 10 th to 12 th 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 e-
mail 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 information: Pneumonia in children (The Basics)" )

SUMMARY AND RECOMMENDATIONS

 The presenting signs and symptoms of community-acquired pneumonia (CAP) are nonspecific;
no single symptom or sign is pathognomonic for pneumonia in children. The combination of
fever and cough is suggestive of pneumonia, but the presentation may be subtle, or misleading
(eg, abdominal pain or nuchal rigidity). (See 'Clinical presentation' above.)
 The history should focus on features that can help to define the clinical syndrome (eg,
pneumonia, bronchiolitis) and narrow the list of potential pathogens (table 1 ).
 (See 'History' above and "Epidemiology, pathogenesis, and etiology of pneumonia in children",
section on 'Etiologic agents' .)
 Examination findings that have been correlated with radiographic pneumonia include tachypnea,
increased work of breathing (retractions, nasal flaring, grunting, use of accessory muscles),
hypoxemia, and adventitious lung sounds. Combinations of findings are more predictive than
single findings. The absence of tachypnea is useful in excluding pneumonia.
(See 'Examination' above.)
 The history and examination are used to determine the severity of illness ( table 3 ), which
determines, in part, the need for radiologic and laboratory evaluation. (See 'Severity
assessment' above.)
 Neither clinical nor radiologic features reliably distinguish between bacterial, atypical bacterial,
and viral pneumonia. (See 'Clues to etiology' above and'Etiologic clues' above.)
 Radiographs are not necessary for children with pneumonia who are well enough to be treated
as outpatients. We suggest that chest radiographs be obtained for the following indications:

 Severe disease ( table 3 ) (see 'Severity assessment' above)

 Confirmation of the diagnosis when clinical findings are inconclusive
 Exclusion of alternate explanations for respiratory distress (see 'Differential diagnosis' above)
 Evaluation for complications (see 'Complications' above)
 Exclusion of occult pneumonia in young children (3 to 36 months) with fever >39ºC,
leukocytosis (white blood cell count >20,000/microL), and no obvious focus of infection
(see 'Radiologic evaluation' above)

 Routine laboratory evaluation is not necessary for children with clinical evidence of mild
uncomplicated lower respiratory tract infection who will be treated as outpatients unless the
findings will help in deciding whether antimicrobial therapy is necessary. (See 'Laboratory
evaluation' above.)
 We recommend that attempts be made to establish an etiologic diagnosis in children with CAP
who require hospital admission. A complete blood count with differential and blood culture
should be obtained in all such patients. If produced, a good quality sputum should be submitted
for Gram stain and culture. Other specimens for microbiologic testing should be obtained as
indicated by the clinical scenario. (See 'Microbiology' above.)
 Attempts also should be made to establish (or exclude) an etiologic diagnosis in patients
suspected to have CAP caused by pathogens that require treatment regimens that differ from
standard empiric regimens. (See 'Critical microbes' above.)
 Alternate diagnoses and coincident conditions must be considered in children who fail to
respond to therapy or who have an unusual presentation or course (table 5 ). (See 'Differential
diagnosis' above and "Outpatient treatment of community-acquired pneumonia in children",
section on 'Treatment failure' and"Inpatient treatment of pneumonia in children" .)
 Complications of CAP in children include pleural effusion and empyema, necrotizing pneumonia,
lung abscess, pneumatocele, and hyponatremia. (See'Complications' above.)

Inpatient treatment of pneumonia in children

INTRODUCTION — Community-acquired pneumonia (CAP) is defined as an acute infection of the
pulmonary parenchyma in a patient who has acquired the infection in the community, as distinguished
from hospital-acquired (nosocomial) pneumonia. CAP is a common and potentially serious illness with
considerable morbidity.

The Pediatric Infectious Diseases Society/Infectious Diseases Society of America and the British
Thoracic Society have developed clinical practice guidelines for the treatment of CAP in children [ 1,2 ].

The inpatient treatment of pneumonia in children will be reviewed here. The outpatient treatment of
CAP is discussed separately, as are the epidemiology, etiology, clinical features, and diagnosis.
(See "Outpatient treatment of community-acquired pneumonia in children" and "Epidemiology,
pathogenesis, and etiology of pneumonia in children" and "Clinical features and diagnosis of
community-acquired pneumonia in children" .)

HOSPITALIZATION

Indications — The decision to hospitalize a child with community-acquired pneumonia (CAP) is

individualized based upon age, underlying medical problems, and clinical factors including severity of
illness ( table 1 ) [ 1-3 ]. Hospitalization generally is warranted for infants younger than three to six
months of age, unless a viral etiology or Chlamydia trachomatis is suspected and they are normoxemic
and relatively asymptomatic. Hospitalization is also warranted for a child of any age whose family
cannot provide appropriate care and assure compliance with the management plan. Additional
indications for hospitalization include [ 1,2 ]:

 Hypoxemia (oxygen saturation [SpO 2 ] <90 percent in room air at sea level)
 Dehydration, or inability to maintain hydration orally; inability to feed in an infant
 Moderate to severe respiratory distress: Respiratory rate >70 breaths/minute for infants <12
months of age and >50 breaths per minute for older children; retractions; nasal flaring;
difficulty breathing; apnea; grunting
 Toxic appearance (more common in bacterial pneumonia and may suggest a more severe
course) [ 4 ]
 Underlying conditions that may predispose to a more serious course of pneumonia (eg,
cardiopulmonary disease, genetic syndromes, neurocognitive disorders), may be worsened by
pneumonia (eg, metabolic disorder) or may adversely affect response to treatment (eg,
immunocompromised host)
 Complications (eg, effusion/empyema)
 Suspicion or confirmation that CAP is due to a pathogen with increased virulence, such as
Staphylococcus aureus or group A streptococcus
 Failure of outpatient therapy (worsening or no response in 48 to 72 hours)

Indications for intensive care — The decision to treat a child with pneumonia in an intensive care
setting is individualized, based upon clinical, laboratory, and radiologic findings. Treatment in an
intensive care setting generally is warranted for children who manifest [ 1,2 ]:

 The need for ventilatory support beyond that which can be provided outside the intensive care
unit (eg, mechanical ventilation, noninvasive positive pressure ventilation, failure to maintain
oxygen saturation [SpO 2 ] >92 percent in FiO 2 >0.5)
 Signs of impending respiratory failure (lethargy, increasing work of
breathing, and/or exhaustion with or without hypercarbia)
 Recurrent apnea or slow irregular respirations
 Cardiovascular compromise with progressive tachycardia and/or hypotension that requires or is
refractory to fluid management

Care in the intensive care unit also may be warranted for children with two or more of the following
[ 1 ]:

 Respiratory rate >70 breaths/minute for infants <12 months of age and >50 breaths per
minute for older children
 Apnea
 Increased work of breathing (retractions, dyspnea, nasal flaring, grunting)
 PaO 2 /FiO 2 ratio <250
 Multilobar infiltrates
 Altered mental status
 Hypotension
 Pleural effusion
 Comorbid condition (eg, sickle cell disease, immune deficiency, immunosuppression)
 Unexplained metabolic acidosis
 Pediatric Early Warning Score >6 [ 5 ]

Infection control — CAP can be caused by a variety of microbial agents requiring a variety of
infection-control measures [ 6 ]. If possible, rapid diagnostic tests should be performed at the time of
admission, to facilitate decisions regarding appropriate precautions. (See "Clinical features and
diagnosis of community-acquired pneumonia in children", section on 'Rapid diagnostic tests' .)

Hand washing is the single most important procedure to prevent the spread of infection. Additional
infection control measures depend upon the likely pathogen(s), as follows [ 6 ]:

 Respiratory syncytial and parainfluenza viruses – gown and gloves (ie, contact precautions)
  Influenza virus, group A streptococcus (for the first 24 hours of treatment), methicillin-
susceptible S. aureus , Bordetella pertussis (until patient has received five days of effective
therapy), and Mycoplasma pneumoniae – mask within 3 feet (ie, droplet precautions)
 Adenovirus – contact and droplet precautions
 Methicillin-resistant S. aureus – special organism precautions; contact and droplet precautions
and dedicated patient equipment

These precautions are discussed separately. (See "General principles of infection control" .) Guidelines
for hand hygiene in healthcare settings can be accessed through the Centers for Disease Control and
Prevention .

SUPPORTIVE CARE — Supportive care includes ensuring adequate antipyresis, analgesia, respiratory
support, and hydration.

Antipyresis and analgesia — Children hospitalized with pneumonia usually have fever and may
have pleuritic chest pain, which can lead to shallow breathing and impaired ability to cough.
Administration of antipyretics and/or analgesics can be used to keep the child comfortable. Adequate
pain control may promote coughing, which facilitates airway clearance. Antitussives should be avoided.
Symptomatic treatment of cough is discussed separately. (See "The common cold in children:
Treatment and prevention", section on 'Cough' .)

Respiratory support — Children hospitalized with pneumonia should receive ventilatory support as
indicated by their clinical condition [ 1,2 ]. A supported sitting position may help to expand the lungs
and improve respiratory symptoms [ 2 ].

We suggest that children with oxygen saturation [SpO 2 ] <95 percent in room air be treated with
supplemental oxygen to maintain oxygen saturation ≥95 percent while they are in respiratory distress.
Different thresholds for supplemental oxygen are suggested by other experts (eg, the British Thoracic
Society guidelines suggest supplemental oxygenation to maintain oxygenation saturation >92 percent)
[ 2 ]. Gentle bulb suction of the nares may be helpful in infants and children whose nares are blocked
with secretions. Minimal handling seems to reduce oxygen requirements. (See "Continuous oxygen
delivery systems for infants, children, and adults" .)

In children who are severely ill, it may be necessary to monitor carbon dioxide tension via blood gas
analysis in addition to oxygen saturation (SpO 2 ) by oximetry. Hypercarbia is an important sign of
impending respiratory failure, particularly in the young infant who is tiring but may have preserved
oxygenation.

Fluid management — Children who cannot maintain adequate fluid intake because of
breathlessness, fatigue, or risk of aspiration [ 7 ] may require intravenous fluid therapy. Nasogastric
(NG) tubes should be avoided if possible because they may compromise breathing; if necessary, the
smallest NG tube possible should be used [ 2 ]. (See "Maintenance fluid therapy in children" .)

Children with pneumonia are at risk for inappropriate secretion of antidiuretic hormone (SIADH)
[ 8,9 ]. Serum electrolytes should be monitored if there is clinical suspicion of SIADH [ 9 ].
(See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion
(SIADH)", section on 'Pulmonary disease' .)

Chest physiotherapy — Chest physiotherapy is not beneficial for children with uncomplicated
community-acquired pneumonia (CAP) [ 2 ]. In randomized and observational studies in children and
adults, chest physiotherapy had no effect on length of hospital stay, duration of fever, or radiographic
resolution [ 10-14 ].

EMPIRIC THERAPY

Overview — The initial treatment of children who are hospitalized with pneumonia is empiric ( table
2 ). Factors that must be considered include the spectrum of likely pathogens, antimicrobial
susceptibility, simplicity, tolerability, palatability, safety, and cost [ 15 ].
The recommendations of most guidelines are based on in vitro susceptibilities of the most likely
pathogen or pathogens, rather than evidence of the superiority of one antibiotic over another. Clinical
response to empiric therapy and results of microbiologic studies, when available, help to determine
whether additional evaluation or changes in therapy are necessary [ 1,2 ]. (See "Clinical features and
diagnosis of community-acquired pneumonia in children", section on 'Microbiology' and 'Specific
therapy' below and 'Response to therapy' below.)

There are few randomized controlled trials to guide the choice of empiric antibiotics in children with
community-acquired pneumonia (CAP). Decisions regarding empiric therapy are complicated by the
substantial overlap in the clinical presentation of bacterial and nonbacterial pneumonias [ 16-18 ].
Treatment decisions usually are based upon algorithms that include patient age, epidemiologic and
clinical information, and diagnostic laboratory and imaging studies ( table 2 ) [ 4 ]. The scope of
empiric therapy (ie, narrow or broad) depends upon the severity of illness and presence of
complications. Agents other than those suggested in the table may be more appropriate if there are
clinical or epidemiologic features strongly suggestive of a specific cause (eg, mediastinal or hilar
lymphadenopathy, residence in the central United States, and exposure to caves and/or bat guano
suggestive of pulmonary histoplasmosis) [ 19 ].

Consultation with a specialist in infectious disease may be helpful in children with medication allergies,
comorbid conditions, failure of outpatient therapy, or multiple-drug-resistant organisms. Consultation
with a pediatric pulmonologist may be helpful in children with recurrent pneumonia. (See "Clinical
features and diagnosis of community-acquired pneumonia in children" and "Outpatient treatment of
community-acquired pneumonia in children", section on 'Treatment failure'.)

Etiologic clues — Certain clinical and epidemiologic features can be used to determine the most
likely pathogen(s) to aid in decisions regarding empiric therapy. Because these features often overlap,
they cannot be used with complete confidence, but are helpful in guiding empiric therapy until results
of microbiologic tests are available ( table 3 ). These features are discussed in greater detail
separately. (See "Clinical features and diagnosis of community-acquired pneumonia in children",
section on 'Clues to etiology' and "Clinical features and diagnosis of community-acquired pneumonia in
children", section on 'Etiologic clues' .)

Neonates — The treatment of neonatal pneumonia is discussed separately. (See "Neonatal

pneumonia" .)

Viral pneumonia — Most children younger than three to five years of age who are admitted to the
hospital with pneumonia have viral pneumonia (eg, respiratory syncytial virus). This is particularly true
in the absence of lobar (or lobular) infiltrate and pleural effusion [ 4 ]. Viral pneumonia does not
require antibiotic therapy, unless a mixed infection or secondary bacterial infection is suspected.
(See "Respiratory syncytial virus infection: Treatment", section on 'Overview' and"Respiratory syncytial
virus infection: Clinical features and diagnosis", section on 'Clinical manifestations' .)

No effective antivirals are available for most viral pneumonias, with the exception of influenza.

Influenza pneumonia — Initiation of antiviral treatment for influenza (eg, oseltamivir ) as soon as
possible is recommended for children hospitalized with presumed influenza pneumonia; laboratory
confirmation should not delay initiation of antiviral therapy. The diagnosis and treatment of influenza in
children are discussed separately. (See "Antiviral drugs for the prevention and treatment of seasonal
influenza in children", section on 'Antiviral therapy' and "Clinical features and diagnosis of seasonal
influenza in children", section on 'Diagnosis' .)

For children with influenza pneumonia in whom secondary bacterial pneumonia is suspected, empiric
antibiotic therapy should include coverage for S. aureus , including methicillin-resistant S.
aureus (MRSA). Coinfection with S. aureus may be particularly severe and rapidly fatal. (See "Clinical
features and diagnosis of seasonal influenza in children", section on 'S. aureus' .)

Uncomplicated bacterial pneumonia — Streptococcus pneumoniae is the most common bacterial

cause of pneumonia in children of all ages [ 4,20 ]. Other potential bacterial pathogens that may need
to be included in empiric therapy for hospitalized children include S. aureus , including methicillin-
resistant S. aureus(MRSA), S. pyogenes (group A streptococcus ), Haemophilus influenzae type b (if
unimmunized), nontypeable H. influenzae , and Moraxella catarrhalis [ 2,4,20-25].

The Table provides several suggested parenteral empiric antibiotic regimens

for uncomplicated bacterial pneumonia in hospitalized children when S. aureus is not a consideration
( table 2 ) [ 4,26,27 ]. The treatment of complicated CAP and severe CAP (particularly when S.
aureus is a consideration) are discussed below. (See'Complicated CAP' below and 'Severe CAP
requiring ICU admission' below.)

Ampicillin or penicillin G generally provides adequate coverage for the fully immunized child in
communities without substantial prevalence of penicillin-resistant S. pneumoniae [ 1 ]. We suggest a
third-generation cephalosporin (eg, cefotaxime , ceftriaxone ) for children younger than 12 months and
those who are not fully immunized because third-generation cephalosporins provide coverage for the
beta-lactamase producing pathogens (eg, H. influenzae and M. catarrhalis ) that may occur in these
children. We also suggest third-generation cephalosporins also for children with more severe illness
( table 1 ) because they provide coverage for a broader range of pathogens, including penicillin-
resistant S. pneumoniae , than does ampicillin [ 1,28,29 ].

A macrolide may be added ( table 2 ) if M. pneumoniae , C. pneumoniae , or legionellosis is suspected.

(See 'Atypical pneumonia' below.)

We suggest that children who require hospitalization for treatment of CAP be treated initially with
parenteral antibiotics. However, oral amoxicillin may be an alternative for children older than six
months with uncomplicated pneumonia that is not thought to be due to S. aureus . In a multicenter
randomized trial, treatment with amoxicillin was equivalent to treatment with penicillin G in children
with CAP who required hospital admission but did not have wheezing, hypotension, chronic pulmonary
conditions (other than asthma), immunodeficiency, pleural effusion requiring drainage, or oxygen
saturations <85 percent in room air [ 30 ]. The British Thoracic Society guidelines suggest that oral
antibiotics are safe and effective even for children with severe pneumonia as long as they are able to
tolerate oral fluids, are not vomiting, and do not have signs of septicemia or complicated pneumonia
[ 2 ].

Atypical pneumonia — Atypical bacterial pathogens include C. trachomatis in afebrile infants, and M.
pneumoniae and C. pneumoniae in older children and adolescents. The Table provides several
suggested empiric regimens for atypical bacterial pneumonia in hospitalized children ( table 2 )
[ 4,26 ].

For children older than four months with presumed atypical bacterial pneumonia, ampicillin or a
second- or third-generation cephalosporin may be added if there is strong evidence of a bacterial cause
(eg, white blood cell count >15,000/microL, CRP >35 to 60 mg/L (3.5 to 6 mg/dL), chills, no response
to outpatient therapy with a macrolide or doxycycline ) [ 4,31 ].

Fluoroquinolones (eg, levofloxacin , moxifloxacin ) may be reasonable empiric therapy for the older
child and adolescent with suspected atypical pneumonia, who could actually have pneumococcal
pneumonia. The fluoroquinolones also may be used in the older child or adolescent who has a type 1
hypersensitivity ( table 4 ) to beta-lactam antibiotics. In addition to their excellent gram-negative
spectrum, the fluoroquinolones are active against a number of the pathogens responsible for CAP,
including beta-lactam-susceptible and nonsusceptible S. pneumoniae , M. pneumoniae (including
macrolide-resistant M. pneumoniae) , and C. pneumoniae [32 ]. However, S. pneumoniae resistant to
levofloxacin have been identified [ 33 ].

Severe CAP — Children with severe CAP that does not require admission to the intensive care unit
( table 1 ) may benefit from combination empiric therapy with a macrolide and a beta-lactam antibiotic
(eg, penicillin or third-generation cephalosporin) ( table 2 ). Combination therapy improves coverage
for resistant organisms and mixed bacterial/atypical bacterial infections. Antimicrobial therapy can be
adjusted as necessary when results of microbiologic testing become available. Invasive diagnostic
testing, including bronchoscopy with bronchoalveolar lavage, may be necessary for specific
microbiologic diagnosis. (See'Uncomplicated bacterial pneumonia' above and 'Atypical
pneumonia' above and "Clinical features and diagnosis of community-acquired pneumonia in children",
section on 'Invasive studies' .)

Severe CAP requiring ICU admission — Children who are admitted to the intensive care unit for
serious or life-threatening infections require broad-spectrum empiric coverage that addresses potential
beta-lactam resistance and community-associated methicillin-resistant S. aureus (CA-MRSA). A
suggested regimen for such children may include ( table 2 ) [ 34-36 ]:

 Vancomycin 60 mg/kg per day IV in four divided doses up to a maximum of 4 g/day, and
 A third-generation cephalosporin ( cefotaxime 150 mg/kg per day IV in four divided doses up to
a maximum of 10 g/day or ceftriaxone 100 mg/kg per day IV in two divided doses up to a
maximum dose of 4 g/day), and
 Azithromycin 10 mg/kg once per day IV for two days (maximum 500 mg/day), followed by
5 mg/kg once per day IV (maximum 250 mg/day), and possibly
 Nafcillin or oxacillin 150 mg/kg per day IV in four divided doses; maximum 12 g/day if S.
aureus is likely (methicillin-susceptible S. aureus is more rapidly killed by nafcillin than
by vancomycin ), and possibly
 Antiviral therapy for influenza, if the child is hospitalized during influenza season; laboratory
confirmation of influenza should not delay initiation of antiviral therapy. (See "Antiviral drugs for
the prevention and treatment of seasonal influenza in children", section on 'Antiviral therapy' .)

This combination is necessary because of reports of treatment failure resulting from treatment of
nonsusceptible S. pneumoniae with beta-lactams, increasingclindamycin resistance among S.
pneumoniae , and concern for MRSA [ 34 ]. Virtually all strains of MRSA are susceptible
to vancomycin [ 35 ]. (See "Treatment of invasive methicillin-resistant Staphylococcus aureus infection
in children", section on 'Pneumonia' .)

When treating with vancomycin , renal function and serum trough levels or dosing to achieve
an AUC/MIC ratio >400 should be monitored in an attempt to assure therapeutic efficacy and limit
toxicity. In adults, vancomycin trough levels between 15 and 20 microgram/mL have been suggested
to improve clinical outcomes for complicated infections due to S. aureus [ 36-38 ].

Linezolid is an oxazolidinone antibiotic with activity against gram-positive cocci, including beta-lactam-
resistant S. pneumoniae and MRSA. Linezolid could be substituted for vancomycin and nafcillin in the
above regimen. The dose for linezolid is 10 mg/kg per dose (maximum 600 mg); it is administered
every eight hours in children younger than 12 years and every 12 hours in children 12 years and older.

Complicated CAP — Complicated CAP (eg, parapneumonic effusion, lung abscess) requires a broader
spectrum of antibiotic coverage if etiologies other than S. pneumoniae are being considered. The
expanded spectrum should include coverage for beta-lactam-resistant isolates and community-
associated methicillin-resistant S. aureus (CA-MRSA). Coverage for anaerobes and gram-negative
organisms also may be necessary for children with lung abscess [ 39 ]. Antimicrobial therapy can be
adjusted as necessary when results of microbiologic testing become available. (See "Clinical features
and diagnosis of community-acquired pneumonia in children", section on
'Complications' and "Management and prognosis of parapneumonic effusion and empyema in
children" .)

Complicated CAP requires a prolonged course of antimicrobial therapy, usually initiated parenterally
[ 19 ]. Appropriate regimens may include [ 26 ]:

 Ceftriaxone 100 mg/kg intravenously (IV) in two divided doses up to a maximum dose of
4 g/day, OR cefotaxime 150 mg/kg per day IV in four divided doses up to a maximum of
10 g/day, PLUS clindamycin 30 to 40 mg/kg per day IV in three or four divided doses to a
maximum of 1 to 2 g/day if S. aureus or anaerobes are a consideration.

Vancomycin 40 to 60 mg/kg per day IV in three or four divided doses up to a maximum of

4 g/day is an alternative to clindamycin if the patient is allergic to clindamycin. When treating
with vancomycin, renal function and serum trough levels or dosing to achieve an AUC/MIC ratio
 of >400 should be monitored in an attempt assure therapeutic efficacy and limit toxicity. In
adults, vancomycin trough levels between 15 and 20 microgram/mL have been suggested to
improve clinical outcomes for complicated infections due to S. aureus [ 36-38 ].
(See "Treatment of invasive methicillin-resistant Staphylococcus aureus infection in children",
section on 'MRSA infections' .)
 Ampicillin-sulbactam 150 to 200 mg/kg per day of the ampicillin component IV in four divided
doses; maximum 12 g/day alone may be effective if a lung abscess is thought to be secondary
to an aspiration event. (See 'Aspiration pneumonia' below.)

The duration of therapy and other considerations in the management of complicated pneumonia
depend upon the type of complication:

 Parapneumonic effusion/empyema – The treatment of parapneumonic effusion and

empyema is discussed in detail separately. (See "Management and prognosis of parapneumonic
effusion and empyema in children" .)
 Necrotizing pneumonia – Treatment of necrotizing pneumonia requires a prolonged course of
antibiotic therapy. The duration is determined by the clinical response but is usually a total of
four weeks or two weeks after the patient is afebrile and has improved clinically. Interventional
procedures (eg, percutaneous drainage catheter placement) should be performed cautiously in
children with necrotizing pneumonia; such procedures increase the risk of complications, such
as the development of bronchopleural fistulae [ 39-42 ].
 Lung abscess – Treatment of lung abscess requires a prolonged course of antibiotic therapy.
The duration is determined by the clinical response, but is usually a total of four weeks or two
weeks after the patient is afebrile and has clinical improvement. The average duration of fever
is four to eight days [ 19 ]. Eighty to 90 percent of lung abscesses in children resolve with
antibiotic therapy alone and spontaneous drainage through the tracheobronchial tree, provided
that bronchial obstruction is removed [ 43 ].

In cases that fail to resolve with antibiotics alone, needle aspiration or percutaneous catheter
drainage may provide diagnostic information and therapeutic benefit without the increased risk
of complications that occurs in children with necrotizing pneumonia [ 39,40,44,45 ].
Percutaneous drainage may be warranted in children with lung abscess whose condition fails to
improve or worsens after 72 hours of antibiotic therapy [ 39 ]. At least three weeks of IV
antibiotic therapy should be delivered before lobectomy is considered for treatment failure
[ 46 ].
 Pneumatocele – Most pneumatoceles involute spontaneously [ 47-49 ]. However, on occasion,
pneumatoceles result in pneumothorax [ 50 ].

Nosocomial pneumonia — Empiric treatment of nosocomial (hospital-acquired) pneumonia should

include coverage for S. aureus , Enterobacteriaceae,Pseudomonas aeruginosa , and anaerobes.
Acceptable broad spectrum regimens usually include an aminoglycoside (for gram-negative pathogens)
and another agent to address gram-positive pathogens and anaerobes ( table 2 ):

 Aminoglycoside (usually gentamicin ; amikacin if extended spectrum or Amp C beta-lactamase

producing gram-negative rods are possible etiologies) plus :
 Ticarcillin-clavulanate 300 mg/kg per day IV in four divided doses up to a maximum of
24 g/day, or
 Piperacillin-tazobactam 300 mg/kg per day IV in four divided doses up to a maximum of
12 g/day, or
 Meropenem 60 mg/kg per day IV in three divided doses, up to a maximum of 6 g/day if
extended-spectrum or Amp C beta-lactamase-producing gram-negative rods are possible
etiologies, or
 Ceftazidime 125 to 150 mg/kg per day in three divided doses; maximum of 6 g/day, or
 Cefepime 150 mg/kg per day in three divided doses; maximum of 4 g/day

The combination of amikacin and meropenem should be used if extended-spectrum or Amp C beta-
lactamase-producing gram-negative rods are possible etiologies.
The cephalosporin/aminoglycoside combination lacks anaerobic coverage so should NOT be used when
aspiration pneumonia is a possibility. (See 'Aspiration pneumonia' below.)
Vancomycin should be added to the empiric regimen if methicillin-resistant S. aureus is a
consideration.

Patients with true beta-lactam hypersensitivity (ie, type 1 hypersensitivity reaction) ( table 4 ) can be
treated with a combination of clindamycin and an aminoglycoside.

Aspiration pneumonia — Empiric antibiotic regimens for community-acquired aspiration pneumonia

must cover oral anaerobes. Appropriate antibiotic regimens for hospitalized children include [ 39 ]:

 Ampicillin-sulbactam 150 to 200 mg/kg per day of the ampicillin component IV in four divided
doses; maximum 12 g/day, or
 Clindamycin 30 to 40 mg/kg per day IV in three or four divided doses to a maximum of 1 to
2 g/day if MRSA etiology is suspected. (See "Treatment of invasive methicillin-resistant
Staphylococcus aureus infection in children", section on 'Pneumonia' .)

In neurologically compromised older adolescents prone to aspiration events, empiric treatment for CAP
with a fluoroquinolone like moxifloxacin (400 mg once daily) may be reasonable. Moxifloxacin has
activity against anaerobic bacteria, as well as the usual treatable causes of CAP ( S. pneumoniae , M.
pneumoniae , and C. pneumoniae) .

Appropriate antibiotic regimens for children with nosocomial aspiration who are known to be colonized
with unusual gram-negative pathogens (eg, Klebsiella pneumoniae ) include:

 Ticarcillin-clavulanate 300 mg/kg per day IV in four divided doses up to a maximum of

24 g/day, or
 Piperacillin-tazobactam 300 mg/kg per day IV in four divided doses up to a maximum of
12 g/day, or
 Meropenem 60 mg/kg per day IV in three divided doses, up to a maximum of 6 g/day

Vancomycin should be added to the empiric regime if methicillin-resistant S. aureus (MRSA) is a

consideration.

Patients with true beta-lactam hypersensitivity (ie, type 1 hypersensitivity reaction) ( table 4 ) can be
treated with a combination of clindamycin and an aminoglycoside.

Immunocompromised host — Empiric treatment for pneumonia in immunocompromised hosts also

requires broad-spectrum gram-positive and gram-negative coverage, similar to that required for
nosocomial pneumonia, with the addition of vancomycin if methicillin-resistant staphylococcus is
considered, and possiblytrimethoprim-sulfamethoxazole for Pneumocystis jirovecii (formerly P. carinii ).
Empiric regimens may need to be modified once results of cultures and antibiotic susceptibility testing
are available. Invasive testing may be required to obtain a satisfactory specimen in such patients.
(See "Clinical features and diagnosis of community-acquired pneumonia in children", section on
'Invasive studies' .) Treatment of CAP in the immunocompromised host should occur in consultation
with an infectious disease specialist.

An aggressive approach to specific microbial diagnosis is indicated in immunocompromised hosts with

clinically significant pneumonias. For patients with an endotracheal tube in place, specific microbial
diagnosis may involve early flexible bronchoscopy for bronchoalveolar lavage with viral, fungal, and
bacterial cultures. Although the protected specimen brush technique has been utilized in some settings,
quantitative bacterial cultures are more commonly used to differentiate colonization from true lower
respiratory tract infection. (See "Flexible bronchoscopy: Indications and contraindications" and "Clinical
presentation and diagnosis of ventilator-associated pneumonia", section on 'Diagnostic evaluation' .)

SPECIFIC THERAPY — Once results of microbiologic tests are available, antimicrobial therapy can be
directed toward the responsible pathogen or pathogens. Specific antibiotic therapy for bacterial CAP is
summarized in the table ( table 5 ). Specific antimicrobial and/or supportive therapy for the pathogens
that commonly cause CAP in children is discussed in the topic reviews listed below.

 S. pneumoniae (see "Pneumococcal pneumonia in children", section on 'Specific therapy' )

  M. pneumoniae (see "Mycoplasma pneumoniae infection in children", section on 'Treatment' )
 C. pneumoniae (see "Pneumonia caused by Chlamydophila (Chlamydia) species in children" )
 Methicillin-sensitive S. aureus – Methicillin-susceptible S. aureus pneumonia may be treated
with oxacillin , nafcillin , or cefazolin [ 1,4 ]
 Methicillin-resistant S. aureus (MRSA) (see "Treatment of invasive methicillin-resistant
Staphylococcus aureus infection in children", section on 'Definitive therapy' )
 Respiratory syncytial virus (see "Respiratory syncytial virus infection: Treatment" )
 Influenza (see "Antiviral drugs for the prevention and treatment of seasonal influenza in
children", section on 'Antiviral therapy' )
 Parainfluenza (see "Parainfluenza viruses in children", section on 'Treatment' )
 Adenovirus (see "Diagnosis and treatment of adenovirus infection", section on 'Treatment' )
 Human metapneumovirus (see "Human metapneumovirus infections", section on 'Treatment' )

DURATION OF TREATMENT

Parenteral therapy — There are few data to guide decisions about the duration of parenteral therapy
for community-acquired pneumonia (CAP) [ 2 ]. It is common to switch to oral therapy in patients who
have received parenteral antibiotics when the patient has become afebrile for 24 to 48 hours and is not
having emesis [ 51 ].

Total duration — There are few randomized controlled trials to guide decisions about the appropriate
duration of antimicrobial therapy for radiographically confirmed childhood pneumonia [ 2 ]. Current
practice assigns duration of therapy according to the host, causative agent, and severity.

Uncomplicated cases — The usual duration of combined parenteral and oral therapy for
uncomplicated pneumonia is 7 to 10 days [ 1,2 ]. Some authorities suggest continuing oral therapy at
least one week beyond resolution of fever; others suggest treating until the erythrocyte sedimentation
rate falls below 20mm/hour. Some data from trials in adults suggest that a shorter course may be
equivalent to a 7- to 10-day course, but additional controlled studies are necessary before this practice
can be recommended routinely for children [ 39,52,53 ].

Complicated cases — Treatment of complications, such as necrotizing pneumonia and lung abscess,
requires a prolonged course of antibiotic therapy, usually initiated parenterally. The duration is
determined by the clinical response, but usually is either a total of four weeks or a total of two weeks
after the patient is afebrile and has improved clinically. (See 'Complicated CAP' above.)

RESPONSE TO THERAPY — The following clinical parameters can be monitored to assess response
to treatment [ 1,2 ]:

 Temperature
 Respiratory rate
 Heart rate
 Oxygen saturation (SpO 2 )
 Work of breathing (eg, retractions, nasal flaring, grunting)
 Chest examination (extent of abnormal or absent breath sounds; extent of dullness to
percussion)
 Mental status
 Ability to maintain oral intake and hydration

The frequency of monitoring depends upon the severity of illness. In patients who are receiving oxygen
supplementation, oxygen saturation should be evaluated regularly. Evaluation for hypercarbia may be
necessary in children with severe respiratory distress, as oxygenation may be preserved.

The respiratory status of children with community-acquired pneumonia (CAP) who are appropriately
treated should improve within 48 to 72 hours [ 1 ]. However, fevers may persist for several days after
initiation of appropriate therapy [ 39 ].

Treatment failure — In children who fail to improve as anticipated, the following possibilities must
be considered [ 1,2,54,55 ]:
  Alternative or coincident diagnoses (eg, foreign body aspiration) (see "Clinical features and
diagnosis of community-acquired pneumonia in children", section on 'Differential diagnosis' )
 Ineffective antibiotic coverage (lack of coverage for the actual etiology or resistant organism)
 Development of complications (see "Clinical features and diagnosis of community-acquired
pneumonia in children", section on 'Complications' )
 Underlying immunodeficiency condition

The history should be reviewed with special attention to the possibility of foreign body aspiration and
geographic or environmental exposures associated with pathogens not treated by the empiric regimen
( table 6 ).

Changes in laboratory parameters (eg, peripheral white blood cell count, inflammatory markers (if
obtained initially)) may provide information about disease progression. Repeat radiographs or
additional imaging studies can help to assess the degree of parenchymal involvement and evaluate for
complications or anatomic abnormalities [ 1 ]. (See "Clinical features and diagnosis of community-
acquired pneumonia in children", section on 'Complications' and "Epidemiology, pathogenesis, and
etiology of pneumonia in children", section on 'Etiologic agents' .)

Depending upon the severity of illness, more aggressive attempts may need to be made to establish a
microbiologic diagnosis (eg, induced sputum [ 56 ], bronchoscopy with bronchoalveolar lavage,
percutaneous needle aspiration, or lung biopsy). In children with lung abscess whose condition fails to
improve or worsens after 72 hours of antibiotic therapy, needle aspiration or percutaneous catheter
drainage may provide diagnostic information and therapeutic benefit [39,40,44,45 ]. (See "Clinical
features and diagnosis of community-acquired pneumonia in children", section on 'Invasive studies' .)

DISCHARGE CRITERIA — Discharge criteria for children who have been admitted to the hospital
with community-acquired pneumonia (CAP) have not been standardized, but typically include [ 1,39 ]:

 Improvement of vital signs

 Ability to maintain adequate fluid and nutrition orally
 Ability to maintain oxygen saturation ≥90 percent in room air
 Improvement in respiratory distress (tachypnea, retractions, nasal flaring, use of accessory
muscles)
 Overall clinical improvement including level of activity, appetite, and decreased fever for at least
12 to 24 hours
 Stable and/or baseline mental status
 Parents’ ability to administer and child’s ability to comply with home antibiotic regimen
 Safe and compliant home environment

Outpatient parenteral antibiotic therapy — Outpatient parenteral antimicrobial therapy (OPAT) is

an option for selected patients who require prolonged treatment (usually for complicated CAP that for
some reason cannot be treated with an oral antibiotic) and have stabilized clinically [ 39,57,58 ].
Eligibility for OPAT requires a suitable home environment and a pharmacologic agent with a reasonable
dosing schedule [ 59 ]. Decisions regarding OPAT should involve the caregivers, an infectious disease
specialist (or clinician knowledgeable about the use of antimicrobial agents in OPAT), a hospital
pharmacist, and the primary care provider. The services of a visiting nurse may be required for home
visits, education and observation of caregiver administration, and/or obtaining blood samples for
therapeutic monitoring.

FOLLOW-UP

Clinical course — Children with pneumonia should be seen by their primary care provider soon after
discharge to ensure that clinical improvement continues and antibiotic therapy is being taken as
prescribed [ 39 ]. Decisions regarding the timing of clinical follow-up should involve the child's primary
care provider and the clinical status of the child at the time of discharge.

Children who are appropriately treated for pneumonia should gradually improve with time. Cough may
persist for as long as three to four months after viral pneumonia or pertussis. Children who are
recovering from typical or atypical bacterial pneumonia may continue to cough for several weeks and
have moderate dyspnea on exertion for two to three months [ 60 ]. Symptomatic treatment of cough is
discussed separately. (See "The common cold in children: Treatment and prevention", section on
'Cough' .)

Radiographs — Follow-up radiographs are not necessary in asymptomatic children with

uncomplicated community-acquired pneumonia (CAP). However, in children with complicated
community-acquired pneumonia or CAP that required intervention, follow-up radiographs help to
ensure resolution [ 2,61 ]. Follow-up radiographs also may be helpful in children with recurrent
pneumonia, persistent symptoms, severe atelectasis, unusually located infiltrates, or round pneumonia
[2,39,62 ]. Conditions that must be considered if a round pneumonia fails to resolve on follow-up
imaging include congenital lung sequestration, metastatic Wilms tumor, cavitary necrosis, pleural
pseudocyst, and primary lung carcinoma [ 62-66 ]. When follow-up radiographs are indicated, they
should be obtained two to three weeks after hospital discharge [ 39,67 ].

Several studies have evaluated the utility of follow-up radiographs in cohorts of children with acute
radiologically proven CAP [ 68-73 ]. Three of the studies included clinical as well as radiologic follow-up
at three to seven weeks after initial diagnosis [ 68-71 ]. In each of these studies, follow-up
radiographs were normal or improved in asymptomatic children. Residual findings, even when present,
did not result in additional therapy.

PROGNOSIS — Most otherwise healthy children with pneumonia recover without sequelae, even if
the pneumonia is complicated [ 39,41,42,74 ]. Although some data suggest that nearly one-half of
children who are hospitalized for viral pneumonia have symptoms of asthma five years after
hospitalization, it is not clear whether this is related to unrecognized asthma at the time of
presentation with pneumonia or a tendency to develop asthma after viral community-acquired
pneumonia (CAP) [ 75,76 ].

The overall pneumonia mortality rate in developed countries is <1 per 1000 per year [ 77 ].
Pneumococcal pneumonia case fatality rates (not adjusted for comorbid conditions) for children in the
United States were estimated to be 4 percent in children younger than two years and 2 percent in
children 2 to 17 years [78 ].

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 5 th to 6 th 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 10 th to 12 th 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 e-
mail 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 topics (see "Patient information: Pneumonia in children (The Basics)" )

SUMMARY AND RECOMMENDATIONS

 The decision to hospitalize a child with community-acquired pneumonia (CAP) must be

individualized and is based upon age, underlying medical problems, and severity of illness
( table 1 ). (See 'Indications' above.)
 CAP can be caused by a variety of microbial agents requiring a variety of infection-control
measures. (See 'Infection control' above.)
 Supportive care for children hospitalized with pneumonia includes provision of adequate
respiratory support, hydration, antipyresis, and analgesia. (See'Supportive care' above.)
 Children with CAP who are hospitalized are treated empirically until information from the
microbiologic evaluation is available to direct therapy toward a specific pathogen. Decisions
regarding empiric antimicrobial therapy for CAP in children are usually based upon age unless
there are other overriding epidemiologic or clinical factors to suggest a specific etiologic agent
 ( table 2 ). (See 'Overview' above and "Epidemiology, pathogenesis, and etiology of pneumonia
in children", section on 'Etiologic agents' .)
 We recommend that empiric antibiotic therapy for presumed bacterial pneumonia in hospitalized
children include coverage for Streptococcus pneumoniae (table 2 ) ( Grade 1B ).
(See 'Uncomplicated bacterial pneumonia' above.)
 Extended empiric coverage may be indicated for children with complicated or severe
pneumonia, particularly those who require admission to an intensive care unit ( table 2 ).
(See 'Complicated CAP' above and 'Severe CAP requiring ICU admission' above.)
 When results of microbiologic tests are available, antibiotic therapy can be directed toward the
specific pathogen recovered ( table 5 ). (See 'Specific therapy'above.)
 Oral therapy typically is initiated when the patient has been afebrile for 24 to 48 hours and can
tolerate oral intake. The total duration of antibiotic therapy is usually 7 to 10 days for
uncomplicated CAP and up to four weeks in complicated CAP. (See 'Duration of
treatment' above.)
 The respiratory status of children receiving appropriate therapy for CAP should improve within
48 to 72 hours. Children who fail to improve as anticipated may be receiving inadequate
antibiotic therapy, have developed complications, or have an alternative or coincident diagnosis.
(See 'Treatment failure' above.)
 Children recovering from CAP may continue to have cough for several weeks to four months,
depending upon the etiology. Those recovering from typical or atypical bacterial pneumonia
may have moderate dyspnea on exertion for two to three months. (See 'Clinical course' above.)
 Follow-up radiographs are not necessary in asymptomatic children with uncomplicated CAP.
However, in children with complicated CAP or CAP that required intervention, follow-up
radiographs help to ensure resolution. Follow-up radiographs two to three weeks after
completion of therapy may be helpful in children with recurrent pneumonia, persistent
symptoms, severe atelectasis, round pneumonia, or unusually located infiltrates.
(See 'Radiographs' above.)
 Most otherwise healthy children who develop pneumonia recover without any long-term
sequelae. (See 'Prognosis' above.)

Outpatient treatment of community-acquired pneumonia in children

INTRODUCTION — Community-acquired pneumonia (CAP) is defined as an acute infection of the
pulmonary parenchyma in a patient who has acquired the infection in the community, as distinguished
from hospital-acquired (nosocomial) pneumonia. CAP is a common and potentially serious illness with
considerable morbidity.

The Pediatric Infectious Diseases Society/Infectious Diseases Society of America and the British
Thoracic Society have developed clinical practice guidelines for the evaluation and treatment of CAP in
children [ 1,2 ].

The outpatient treatment of CAP in infants and children will be reviewed here. Neonatal pneumonia and
inpatient treatment of pneumonia are discussed separately, as are the epidemiology, etiology, clinical
features, and diagnosis. (See "Neonatal pneumonia" and "Inpatient treatment of pneumonia in
children" and"Epidemiology, pathogenesis, and etiology of pneumonia in children" and "Clinical
features and diagnosis of community-acquired pneumonia in children" .)

INDICATIONS FOR HOSPITALIZATION — The decision to hospitalize a child with community-

acquired pneumonia (CAP) is individualized based upon age, underlying medical problems, and clinical
factors including severity of illness ( table 1 ) [ 1-3 ]. Hospitalization generally is warranted for infants
younger than three to six months of age, unless a viral etiology or Chlamydia trachomatis is suspected
and they are normoxemic and relatively asymptomatic. Hospitalization is also warranted for a child of
any age whose family cannot provide appropriate care and assure compliance with the therapeutic
regimen. Additional indications for hospitalization include [ 1,2 ]:

 Hypoxemia (oxygen saturation <90 percent in room air at sea level)

 Dehydration, or inability to maintain hydration orally; inability to feed in an infant
 Moderate to severe respiratory distress: Respiratory rate >70 breaths per minute for infants
<12 months of age and >50 breaths per minute for older children; retractions; nasal flaring;
difficulty breathing; apnea; grunting
  Toxic appearance (more common in bacterial pneumonia and may suggest a more severe
course) [ 4 ]
 Underlying conditions that may predispose to a more serious course of pneumonia (eg,
cardiopulmonary disease, genetic syndromes, neurocognitive disorders), may be worsened by
pneumonia, even viral pneumonia (eg, metabolic disorder) or may adversely affect response to
treatment (eg, immunocompromised host)
 Complications (eg, effusion/empyema) (see "Epidemiology; clinical presentation; and evaluation
of parapneumonic effusion and empyema in children" and"Management and prognosis of
parapneumonic effusion and empyema in children" )
 Suspicion or confirmation that CAP is due to a pathogen with increased virulence, such as
Staphylococcus aureus or group A streptococcus
 Failure of outpatient therapy (worsening or no response in 48 to 72 hours) (see 'Treatment
failure' below)

EMPIRIC THERAPY

Overview — Children with community acquired pneumonia (CAP) who are treated in the outpatient
setting typically are treated empirically; tests to identify a microbiologic etiology are not recommended
for most children who are well enough to be treated in the outpatient setting [ 1,2 ]. Decisions
regarding empiric therapy are complicated by the substantial overlap in the clinical presentation of
bacterial and nonbacterial pneumonias [ 2,5,6 ]. Treatment decisions are usually based upon
algorithms that include patient age ( table 2 ), epidemiologic and clinical information, and diagnostic
laboratory and imaging studies (if such studies were obtained) [ 4 ]. Consultation with a specialist in
infectious disease may be helpful in children with medication allergies or comorbid conditions.
(See "Clinical features and diagnosis of community-acquired pneumonia in
children" and "Epidemiology, pathogenesis, and etiology of pneumonia in children", section on
'Etiologic agents' .)

There are few randomized controlled trials to guide the choice of empiric antibiotics in children with
CAP. Factors that must be considered include the spectrum of likely pathogens, antimicrobial
susceptibility, simplicity, tolerability, palatability, safety, and cost [ 7 ]. The recommendations of most
guidelines are based upon observations regarding the susceptibility of the most likely pathogen or
pathogens, rather than on evidence of the superiority of one antibiotic over another [ 1,2 ]. The clinical
response to the most commonly used antimicrobials appears to be similar, regardless of etiology
[ 8,9 ]. The response within the first 48 to 72 hours of empiric therapy (or lack of therapy if viral
etiology is most likely) helps to determine whether additional evaluation or changes in therapy are
necessary. (See'Monitoring response' below.)

Children <5 years

Neonates — The treatment of neonatal pneumonia is discussed separately. (See "Neonatal

pneumonia" .)

One to six months — Infants younger than three to six months of age with suspected bacterial CAP
or who are hypoxemic (oxygen saturation <90 percent in room air at sea level) should be admitted to
the hospital for empiric therapy. (See "Inpatient treatment of pneumonia in children", section on
'Empiric therapy' .)

In afebrile infants one to four months of age with CAP, the most likely bacterial pathogen is C.
trachomatis (ie, "afebrile pneumonia of infancy") [ 4,10 ]. Infants who are thought to have afebrile
pneumonia of infancy can be treated in the outpatient setting if they are not hypoxemic and remain
afebrile [ 4 ]. (See"Chlamydia trachomatis infections in the newborn", section on 'Treatment' .)

Bordetella pertussis is a less common, but more severe, cause of pneumonia in young infants; fever
may or may not be present. Like C. trachomatis , B. pertussisis susceptible to the macrolides [ 4 ].
However, young infants who are thought to have B. pertussis -associated pneumonia should be
admitted to the hospital because they are at risk for complications (eg, hypoxia, apnea, pulmonary
hypertension, etc). (See "Treatment and prevention of Bordetella pertussis infection in infants and
children", section on 'Hospitalization' and "Clinical features and diagnosis of Bordetella pertussis
infection in infants and children", section on 'Pneumonia' .)

Six months to five years

Viral pneumonia — Viral etiologies predominate during early childhood, and apparent viral
pneumonia (ie, gradual onset, preceding upper airway symptoms, diffuse findings on auscultation, lack
of toxic appearance) should not be treated with antibiotics. (See "Clinical features and diagnosis of
community-acquired pneumonia in children", section on 'Clues to etiology' and "Epidemiology,
pathogenesis, and etiology of pneumonia in children", section on 'Etiologic agents' .)

No effective antivirals are available for most viral pneumonias, with the exception of influenza.
Initiation of antiviral treatment for influenza (eg, oseltamivir ) as soon as possible is recommended for
children at high risk for complications of influenza pneumonia ( table 3 ); laboratory confirmation
should not delay initiation of antiviral therapy. The diagnosis and treatment of influenza in children are
discussed separately. (See "Antiviral drugs for the prevention and treatment of seasonal influenza in
children", section on 'Antiviral therapy' and "Clinical features and diagnosis of seasonal influenza in
children", section on 'Clinical features' .)

Infants and young children with known or suspected chronic disease (eg, bronchopulmonary disease,
neuromuscular disease, etc) are at increased risk for severe or complicated viral lower respiratory tract
infection (LRTI). If such children are not admitted to the hospital, they merit close monitoring in the
outpatient setting.

Bacterial pneumonia — Streptococcus pneumoniae is the most frequent cause of "typical" bacterial
pneumonia in children of all ages [ 1,2 ]. Bacterial pneumonia in preschool children usually causes
more severe infection, with abrupt onset and moderate to severe respiratory distress, which may
require inpatient therapy. (See 'Indications for hospitalization' above and "Inpatient treatment of
pneumonia in children", section on 'Empiric therapy' .)

For children younger than five years who are thought to have bacterial CAP based upon clinical
presentation, examination findings, and supportive radiographic or laboratory data if obtained (eg,
lobar consolidation on radiograph, white blood cell count [WBC] >15,000/microL, C-reactive protein
>35 to 60 mg/L [3.5 to 6mg/dL]), but do not require inpatient therapy, amoxicillin is usually
considered the drug of choice [ 1,2 ]. We suggest high dose amoxicillin (90 to 100 mg/kg per day
divided into two or three doses; maximum dose 4 g/day) ( table 2 ).

Amoxicillin is preferred because it is effective against the majority of bacterial pathogens for CAP in
this age group, is well tolerated, and is inexpensive [ 1,2 ]. The higher dose of amoxicillin is suggested
because of the increasing prevalence of antibiotic-resistant S. pneumoniae isolated from patients with
community-acquired respiratory tract infections [ 11,12 ]. Amoxicillin is more active in vitro than any
of the oral cephalosporins against these isolates. Universal infant immunization with the 7-valent
pneumococcal conjugate vaccine (PCV7) resulted in a decreased prevalence of penicillin resistant
pneumococci. However, it was associated with the emergence of antibiotic-resistant invasive
serotypes, some of which are included in the 13-valent pneumococcal conjugate vaccine (PCV13) (eg,
serotype 19A) [ 1 ]. The effects of PCV13 on antibiotic resistance have yet to be determined; pending
that information, we continue to suggest high-dose rather than standard dose amoxicillin (ie, 40 to
45 mg/kg per day) when amoxicillin is used to treat CAP in children. (See "Resistance of Streptococcus
pneumoniae to beta-lactam antibiotics" and "Resistance of Streptococcus pneumoniae to the
macrolides, azalides, lincosamines, and ketolides" .)

Although there are prospective, comparative data supporting the efficacy of twice daily dosing
of amoxicillin for the treatment of acute otitis media [ 13-15 ], similar data are not available for
documented pneumococcal pneumonia in children. Unless the etiologic agent is identified as a S.
pneumoniae isolate with a minimum inhibitory concentration (MIC) of <2 mcg/mL, dividing the total
daily 90 to 100 mg/kg dose of amoxicillin into three doses may be warranted. Twice daily dosing for
pneumonia due to a S. pneumoniae isolate with an MIC of 2 mcg/mL is predicted to achieve a clinical
and microbiologic cure in only 65 percent of children, whereas the same total daily dose divided in
three equal portions is predicted to achieve a cure in 90 percent [ 16 ].

For children with non-type 1 hypersensitivity reactions to penicillin ( table 4 ), second or third
generation cephalosporins (eg, cefdinir ) is an acceptable alternative to amoxicillin [ 1 ]. For children
with type 1 hypersensitivity reactions ( table 4 ) to penicillin, clindamycin or a macrolide may be used
[ 1,2 ]. However, if local resistance rates are high for clindamycin and
macrolides, linezolid or levofloxacin may be preferable. Doses are provided in the table ( table 2 ).

For the infant or child who is suspected to have bacterial CAP and is unable to tolerate liquids at the
time of presentation, a single initial dose of ceftriaxone (50 to 75 mg/kg) may be administered
intramuscularly or intravenously before starting oral antibiotics [ 17,18 ].

Atypical pneumonia — Mycoplasma pneumoniae and Chlamydophila pneumoniae are less common
than S. pneumoniae in children younger than five years with CAP [ 5 ]. However, they can occur in this
age group and should be considered in children without a pneumonia-associated complication who fail
to improve after 48 to 72 hours of empiric therapy for S. pneumoniae (eg, amoxicillin ), at which time
a macrolide could be added or substituted ( table 2 ). (See'Treatment failure' below.)

Children ≥5 years

Typical and atypical bacterial pneumonia — Streptococcus pneumoniae is the most frequent
cause of "typical" bacterial pneumonia in children of all ages [1,2 ]. However, in otherwise healthy
children five years and older with CAP who are not ill enough to require hospitalization, M.
pneumoniae and C. pneumoniae are the most likely pathogens [ 4,10,19 ].

We suggest macrolide antibiotics for initial empiric therapy for CAP in children older than five years
who are treated as outpatients [ 1,4 ]. However, the prevalence of macrolide-resistant M.
pneumoniae is increasing in some geographic regions, including Asia, Europe, Israel, and the United
States [ 20-27 ]. The reported prevalence of resistance among M. pneumoniae isolates ranges from
approximately 10 percent in the US to 90 percent in China [ 22,25 ]. Levofloxacin is an alternative for
children >6 months and doxycycline for children >8 years [ 1 ]. The British Thoracic Society clinical
practice guideline suggests amoxicillin as the first-line therapy for children of all ages [ 2 ]. Doses are
provided in the table ( table 2 ).

Among the macrolide antibiotics, clarithromycin and azithromycin have a more convenient dosing
schedule and fewer side effects than erythromycin , but erythromycin is less expensive [ 8,28,29 ].
Macrolide antibiotics may provide coverage for S. pneumoniae , which is the most frequent typical
bacterial pathogen for all age groups [ 30-32 ]. However, approximately 50 percent of S.
pneumoniae isolates are resistant to macrolides. Failure to respond to macrolide therapy may indicate
the development of a complication, a macrolide-resistant pathogen, and/or the need to alter therapy to
provide better pneumococcal coverage. (See'Treatment failure' below.)

Given the significant resistance of S. pneumoniae to macrolides, fluoroquinolones

(eg, levofloxacin , moxifloxacin ) are another reasonable alternative for the outpatient treatment of
CAP in skeletally mature patients. In addition to their excellent gram-negative spectrum, the
fluoroquinolones are active against a number of the pathogens responsible for CAP, including beta-
lactam-susceptible and non-susceptible S. pneumoniae , M. pneumoniae , and C. pneumoniae [ 33 ].
However,S. pneumoniae resistant to levofloxacin has been identified [ 34 ].

Influenza — Initiation of antiviral treatment for influenza (eg, oseltamivir ) as soon as possible is
recommended for children at high risk for complications of influenza pneumonia ( table 3 ); laboratory
confirmation should not delay initiation of antiviral therapy. The diagnosis and treatment of influenza in
children are discussed separately. (See "Clinical features and diagnosis of seasonal influenza in
children" and "Antiviral drugs for the prevention and treatment of seasonal influenza in children",
section on 'Antiviral therapy' .)
Aspiration pneumonia — Community-acquired aspiration pneumonia is usually treated
with amoxicillin-clavulanate . Clindamycin is an alternative for patients allergic to penicillin. Doses are
provided in the table ( table 2 ).

In neurologically compromised skeletally mature adolescents who may be prone to aspiration events,
empiric treatment with moxifloxacin (400 mg once per day) is an alternative. Moxifloxacin is active
against anaerobic bacteria, as well as the usual treatable causes of CAP: S. pneumoniae , M.
pneumoniae , and C. pneumoniae.

Duration — No randomized controlled trials have been performed to determine the appropriate
duration of antimicrobial therapy in radiographically confirmed childhood pneumonia [ 2 ]. Current
practice in the developed world determines the duration of therapy based upon the age of the host,
likely causative agent, and severity of disease:

 We suggest that infants ≥4 months and children with uncomplicated pneumonia suspected or
confirmed to be caused by routine pathogens (ie, S. pneumonia, M. pneumonia , C.
pneumoniae ) be treated for 7 to 10 days; the course of azithromycin is five days [ 1,8 ]
 The duration of treatment for C. trachomatis pneumonia in young infants is discussed
separately (see "Chlamydia trachomatis infections in the newborn", section on 'Treatment' )

A meta-analysis found three days of oral antimicrobial therapy to be as effective as five days for
nonsevere community-acquired pneumonia in children aged 2 to 59 months [ 35 ]. However, the
studies included in the meta-analysis were performed in developing countries, where it is not feasible
to perform radiographs or evaluation for microbiologic etiology; pneumonia was diagnosed by the
World Health Organization (WHO) criteria, which are based on clinical findings and respiratory rate
thresholds. In another study, only 14 percent of children diagnosed with nonsevere pneumonia by the
WHO criteria had radiographic evidence of pneumonia [ 36 ]. Many of the children in the meta-analysis
probably had viral pneumonia, for which antibiotic therapy is not warranted. This is supported by a
subsequent randomized trial in which the clinical outcomes did not differ for children aged 2 to 59
months who were diagnosed with nonsevere pneumonia by the WHO criteria and treated for three days
with amoxicillin versus placebo [ 37 ].

Monitoring response — Children with CAP who are treated as outpatients (including those who were
not initially treated with antibiotics) should have follow-up within 24 to 48 hours [ 1,2 ]. Follow-up may
be performed by phone. Children with CAP who are appropriately treated generally show signs of
improvement within 48 to 72 hours.

Treatment failure — Among patients who do not improve as anticipated, the following possibilities
must be considered [ 1,2,12,38 ]:

 Alternative or coincident diagnoses (eg, foreign body aspiration) (see "Clinical features and
diagnosis of community-acquired pneumonia in children", section on 'Differential diagnosis' )
 Development of complications (see "Clinical features and diagnosis of community-acquired
pneumonia in children", section on 'Complications' )
 Ineffective antibiotic coverage (lack of coverage for the actual etiology or resistant organism)

Worsened condition — Patients whose condition has worsened require additional evaluation and
hospitalization. They also should undergo radiologic evaluation to look for the development of
complications. Laboratory tests should be performed to try to establish a microbiologic diagnosis.
(See "Clinical features and diagnosis of community-acquired pneumonia in children", section on
'Laboratory evaluation' and "Inpatient treatment of pneumonia in children", section on
'Hospitalization' .)

Failure to improve — In patients who fail to improve, but have not worsened, it may be reasonable
to add or strengthen coverage for S. pneumoniae or atypical bacteria if these organisms were not
covered in the initial therapy ( table 2 ) [ 1,4 ]. It is also important to consider underlying or comorbid
conditions (eg, immunodeficiency, anatomic abnormality). (See "Clinical features and diagnosis of
community-acquired pneumonia in children", section on 'Differential diagnosis' .)
Failure to improve while being treated with a beta-lactam antibiotic ( amoxicillin or cephalosporin) may
indicate infection caused by penicillin-resistant S. pneumoniae or S. aureus (either methicillin-
susceptible or -resistant) [ 39 ]. If penicillin-resistant S. pneumoniae is suspected, a change in
antibiotic therapy toclindamycin or linezolid may be indicated. Levofloxacin is an option if there is a
high rate of pneumococcal resistance to clindamycin. Doses are provided in the Table ( table 2 ). If S.
aureus is suspected, the child should be hospitalized. (See "Inpatient treatment of pneumonia in
children" .)

Failure to improve while being treated with a macrolide antibiotic may indicate the need to alter
therapy to provide better coverage for S. pneumoniae or macrolide-resistant M. pneumoniae . For
patients initially treated with macrolides, better pneumococcal coverage can be achieved by the
addition of high-doseamoxicillin , a cephalosporin (eg, cefdinir , cefpodoxime ), or clindamycin . Among
these options, we prefer high-dose amoxicillin because it is well tolerated and inexpensive. Amoxicillin
and cephalosporins may provide coverage for other potential, albeit less common causes, of bacterial
pneumonia in older children (eg,Haemophilus influenza type b, nontypeable H. influenzae , Moraxella
catarrhalis , group A streptococcus ) [ 10 ]. Clindamycin provides coverage for S. aureus . For children
who have type 1 hypersensitivity ( table 4 ) to penicillins, a fluoroquinolone
(eg, levofloxacin , moxifloxacin ) may be used. Tetracyclines (eg, doxycycline ) and fluoroquinolones
can be used if macrolide-resistant M. pneumoniae is suspected [ 40 ]. Doses are provided in the Table
( table 2 ). (See "Mycoplasma pneumoniae infection in children", section on 'Treatment' .)

SUPPORTIVE CARE — The families of children who are managed as outpatients should be instructed
regarding management of fever and pain, maintaining adequate hydration, and identification of
deterioration (eg, persistent fever, increased retractions, use of accessory muscles, grunting, inability
to feed) [ 2 ].

 Children with pneumonia usually have fever and may have pleuritic chest pain, which can lead
to shallow breathing and impaired ability to cough [ 2 ]. Administration of
antipyretics and/or analgesics can be used to keep the child comfortable. Adequate pain control
may promote coughing, which facilitates airway clearance. Antitussives should be avoided as
none have been found to be effective in pneumonia. Symptomatic treatment of cough is
discussed separately. (See "The common cold in children: Treatment and prevention", section
on 'Cough' .)
 Infants and young children with respiratory distress may be better able to maintain hydration if
fluids are provided in small volumes more frequently than in large volumes less often.
 Gentle suction of the nares may be helpful in infants and children whose nares are blocked by
nasal secretions.

FOLLOW-UP

Clinical course — Children who are appropriately treated for community-acquired pneumonia (CAP)
gradually improve with time [ 41 ]. Cough after pertussis commonly persists for many weeks and up to
four months after infection. The symptoms associated with viral lower respiratory tract infections,
particularly cough, usually resolve in less than one month in healthy infants and children, but may
rarely last for up to three to four months. Cough may persist for as long as three to four months after
viral pneumonia or pertussis. Children who are recovering from typical or atypical bacterial pneumonia
may continue to cough for several weeks and have moderate dyspnea on exertion for two to three
months [ 41 ].

Radiographs — Follow-up radiographs are not necessary in asymptomatic children with

uncomplicated CAP. Follow-up radiographs two to three weeks after completion of therapy may be
helpful in assessing alternate diagnoses or coincident conditions in children with recurrent pneumonia,
persistent symptoms, severe atelectasis, unusually located infiltrates, or round pneumonia [ 1,2,42 ].
Conditions that must be considered if a round pneumonia fails to resolve on follow-up imaging include
congenital lung sequestration, metastatic Wilms tumor, cavitary necrosis, pleural pseudocyst, and
primary lung carcinoma [ 42-46 ]. (See "Clinical features and diagnosis of community-acquired
pneumonia in children", section on 'Differential diagnosis' .)
Several studies have evaluated the utility of follow-up radiographs in cohorts of children with acute
radiologically proven CAP [ 47-52 ]. Three of the studies included clinical as well as radiologic follow-up
at three to seven weeks after initial diagnosis [ 47-50 ]. In each of these studies, follow-up
radiographs were normal or improved in asymptomatic children. Residual findings, even when present,
did not result in additional therapy.

PROGNOSIS — Most otherwise healthy children who develop pneumonia recover without any long-
term sequelae [ 32 ]. Although some data suggest that nearly one-half of children who are hospitalized
for viral pneumonia have symptoms of asthma five years after hospitalization, it is not clear whether
this is related to unrecognized asthma at the time of presentation with pneumonia or a tendency to
develop asthma after viral community-acquired pneumonia (CAP) [ 53 ].

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 5 th to 6 th 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
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sophisticated, and more detailed. These articles are written at the 10 th to 12 th 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 e-
mail 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 topics (see "Patient information: Pneumonia in children (The Basics)" )

SUMMARY AND RECOMMENDATIONS

 Community-acquired pneumonia (CAP) is defined as an acute infection of the pulmonary

parenchyma in a patient who has acquired the infection in the community. The clinical
manifestations and diagnosis of CAP are discussed separately. (See "Clinical features and
diagnosis of community-acquired pneumonia in children" .)
 The decision to hospitalize a child with pneumonia must be individualized and is based upon
age, underlying medical problems, and severity of illness ( table 1 ). (See 'Indications for
hospitalization' above.)
 Children with CAP who are treated in the outpatient setting are treated empirically. It is not
necessary to identify a microbiologic etiology in children who are well enough to be treated as
outpatients. Decisions regarding empiric antimicrobial therapy for CAP in children are usually
based upon age unless there are other overriding epidemiologic or clinical factors to suggest a
specific etiologic agent. (See 'Overview' above.)
 Infants younger than three to six months of age with suspected bacterial CAP or who are
hypoxemic should be admitted to the hospital for management. Afebrile infants one to four
months of age who are thought to have afebrile pneumonia of infancy (eg, Chlamydia
trachomatis ) can be treated in the outpatient setting if they are not hypoxemic and remain
afebrile. (See "Inpatient treatment of pneumonia in children" and "Chlamydia trachomatis
infections in the newborn" .)
 We recommend that empiric antibiotic therapy for CAP in children six months to five years of
age who are thought to have bacterial pneumonia (eg, abrupt onset, moderate to severe
respiratory distress, and supportive laboratory data if obtained) include coverage
for Streptococcus pneumoniae ( table 2 ) ( Grade 1B ). (See 'Children <5 years' above.)
 We suggest that empiric antibiotic therapy for CAP in children ≥5 years include coverage for
atypical bacteria ( Grade 2B ). (See 'Children ≥5 years' above.)
 In infants and children six months and older, the usual duration of antimicrobial therapy is five
days for azithromycin and 7 to 10 days for other agents. (See'Duration' above.)
 Children who are treated for CAP as outpatients should have follow-up within 24 to 48 hours.
Those whose condition has worsened at follow-up should be evaluated for potential
complications and hospitalized. (See 'Monitoring response' above and "Inpatient treatment of
pneumonia in children" .)
 Children recovering from CAP may continue to cough for several weeks to four months,
depending upon the etiology. Those recovering from typical or atypical bacterial pneumonia
may have moderate dyspnea on exertion for two to three months. (See 'Clinical course' above.)
 Follow-up radiographs in children with uncomplicated CAP who remain asymptomatic are not
needed. Follow-up radiographs two to three weeks after completion of therapy may be helpful
in children with recurrent pneumonia, persistent symptoms, severe atelectasis, unusually
located infiltrates, or round pneumonia. (See 'Radiographs' above.)
 Most otherwise healthy children who develop pneumonia recover without any long-term
sequelae. (See 'Prognosis' above.)