Official reprint from UpToDate www.uptodate.

com
2013 UpToDate
Print|Back

Epidemiology, pathogenesis, and etiology of pneumonia in children

Author
William J Barson, MD
Section Editor
Sheldon L Kaplan, MD
Deputy Editor
Mary M Torchia, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2013. |This topic last updated: ene 9, 2013.
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
(figure 2) 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. (See "Prevention of Haemophilus influenzae infection", section on 'Efficacy/effectiveness'.)
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 and Staphylococcus aureus pneumonia

Necrotizing pneumonia (associated with aspiration pneumonia and pneumonia resulting from S. pneumoniae, S.
pyogenes, and S. aureus)

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

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, and Achromobacter 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 3). (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 3),
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
th

th

the Basics. The Basics patient education pieces are written in plain language, at the 5 to 6 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
th

th

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 to 12 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.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES

1. Rudan I, Boschi-Pinto C, Biloglav Z, et al. Epidemiology and etiology of childhood pneumonia. Bull World Health Organ
2008; 86:408.
2. Harris M, Clark J, Coote N, et al. British Thoracic Society guidelines for the management of community acquired
pneumonia in children: update 2011. Thorax 2011; 66 Suppl 2:ii1.
3. Margolis P, Gadomski A. The rational clinical examination. Does this infant have pneumonia? JAMA 1998; 279:308.
4. Fiore AE, Shay DK, Broder K, et al. Prevention and control of seasonal influenza with vaccines: recommendations of the
Advisory Committee on Immunization Practices (ACIP), 2009. MMWR Recomm Rep 2009; 58:1.
5. Jokinen C, Heiskanen L, Juvonen H, et al. Incidence of community-acquired pneumonia in the population of four
municipalities in eastern Finland. Am J Epidemiol 1993; 137:977.
6. Wardlaw T, Salama P, Johansson EW, Mason E. Pneumonia: the leading killer of children. Lancet 2006; 368:1048.
7. Glezen P, Denny FW. Epidemiology of acute lower respiratory disease in children. N Engl J Med 1973; 288:498.
8. Boyer KM. Nonbacterial pneumonia. In: Textbook of Pediatric Infectious Diseases, 6th, Feigin RD, Cherry JD, DemmlerHarrison GJ, Kaplan SL (Eds), Saunders, Philadelphia 2009. p.289.
9. Pelton SI, Hammerschlag MR. Overcoming current obstacles in the management of bacterial community-acquired
pneumonia in ambulatory children. Clin Pediatr (Phila) 2005; 44:1.
10. Green GM, Carolin D. The depressant effect of cigarette smoke on the in vitro antibacterial activity of alveolar
macrophages. N Engl J Med 1967; 276:421.
11. MacGregor RR. Alcohol and immune defense. JAMA 1986; 256:1474.
12. Kaplan SL, Mason EO Jr, Wald ER, et al. Decrease of invasive pneumococcal infections in children among 8 children's
hospitals in the United States after the introduction of the 7-valent pneumococcal conjugate vaccine. Pediatrics 2004;
113:443.
13. Grijalva CG, Nuorti JP, Arbogast PG, et al. Decline in pneumonia admissions after routine childhood immunisation with
pneumococcal conjugate vaccine in the USA: a time-series analysis. Lancet 2007; 369:1179.
14. Zhou F, Kyaw MH, Shefer A, et al. Health care utilization for pneumonia in young children after routine pneumococcal
conjugate vaccine use in the United States. Arch Pediatr Adolesc Med 2007; 161:1162.
15. Kronman MP, Hersh AL, Feng R, et al. Ambulatory visit rates and antibiotic prescribing for children with pneumonia, 19942007. Pediatrics 2011; 127:411.
16. Resti M, Moriondo M, Cortimiglia M, et al. Communityacquired bacteremic pneumococcal pneumonia in children:
diagnosis and serotyping by realtime polymerase chain reaction using blood samples. Clin Infect Dis 2010; 51:1042.
17. Blaschke AJ, Heyrend C, Byington CL, et al. Molecular analysis improves pathogen identification and epidemiologic study
of pediatric parapneumonic empyema. Pediatr Infect Dis J 2011; 30:289.
18. Madhi SA, Klugman KP, Vaccine Trialist Group. A role for Streptococcus pneumoniae in virus-associated pneumonia. Nat
Med 2004; 10:811.
19. Mani CS, Murray DL. Acute pneumonia and its complications. In: Principles and Practice of Pediatric Infectious Diseases,
4th, Long SS, Pickering LK, Prober CG. (Eds), Elsevier Saunders, Edinburgh 2012. p.235.
20. Aherne W, Bird T, Court SD, et al. Pathological changes in virus infections of the lower respiratory tract in children. J Clin
Pathol 1970; 23:7.
21. Klein JO. Bacterial pneumonias. In: Textbook of Pediatric Infectious Diseases, 6th, Feigin RD, Cherry JD, DemmlerHarrison GJ, Kaplan SL (Eds), Saunders, Philadelphia 2009. p.302.
22. Baltimore RS. Pneumonia. In: Pediatric Infectious Diseases: Principles and Practice, 2nd ed, Jenson HB, Baltimore RS
(Eds), WB Saunders, Philadelphia 2002. p.794.
23. Dakhama A, Lee YM, Gelfand EW. Virus-induced airway dysfunction: pathogenesis and biomechanisms. Pediatr Infect
Dis J 2005; 24:S159.
24. Mikami R, Murao M, Cugell DW, et al. International Symposium on Lung Sounds. Synopsis of proceedings. Chest 1987;
92:342.
25. Health Policy and Clinical Effectiveness Department. Cincinnati Children's Hospital Medical Center. Community acquired
pneumonia. www.cincinnatichildrens.org/svc/alpha/h/health-policy/ev-based/pneumonia.htm (Accessed on August 11,
2011).

26. Isaacs D. Problems in determining the etiology of community-acquired childhood pneumonia. Pediatr Infect Dis J 1989;
8:143.
27. Wubbel L, Muniz L, Ahmed A, et al. Etiology and treatment of community-acquired pneumonia in ambulatory children.
Pediatr Infect Dis J 1999; 18:98.
28. Korppi M, Heiskanen-Kosma T, Jalonen E, et al. Aetiology of community-acquired pneumonia in children treated in
hospital. Eur J Pediatr 1993; 152:24.
29. Claesson BA, Trollfors B, Brolin I, et al. Etiology of community-acquired pneumonia in children based on antibody
responses to bacterial and viral antigens. Pediatr Infect Dis J 1989; 8:856.
30. Ruuskanen O, Nohynek H, Ziegler T, et al. Pneumonia in childhood: etiology and response to antimicrobial therapy. Eur J
Clin Microbiol Infect Dis 1992; 11:217.
31. Gendrel D, Raymond J, Moulin F, et al. Etiology and response to antibiotic therapy of community-acquired pneumonia in
French children. Eur J Clin Microbiol Infect Dis 1997; 16:388.
32. Heiskanen-Kosma T, Korppi M, Jokinen C, et al. Etiology of childhood pneumonia: serologic results of a prospective,
population-based study. Pediatr Infect Dis J 1998; 17:986.
33. Numazaki K, Chiba S, Umetsu M, et al. Etiological agents of lower respiratory tract infections in Japanese children. In
Vivo 2004; 18:67.
34. Turner RB, Lande AE, Chase P, et al. Pneumonia in pediatric outpatients: cause and clinical manifestations. J Pediatr
1987; 111:194.
35. Vuori E, Peltola H, Kallio MJ, et al. Etiology of pneumonia and other common childhood infections requiring hospitalization
and parenteral antimicrobial therapy. SE-TU Study Group. Clin Infect Dis 1998; 27:566.
36. Michelow IC, Olsen K, Lozano J, et al. Epidemiology and clinical characteristics of community-acquired pneumonia in
hospitalized children. Pediatrics 2004; 113:701.
37. Cevey-Macherel M, Galetto-Lacour A, Gervaix A, et al. Etiology of community-acquired pneumonia in hospitalized
children based on WHO clinical guidelines. Eur J Pediatr 2009; 168:1429.
38. Bradley JS. Management of community-acquired pediatric pneumonia in an era of increasing antibiotic resistance and
conjugate vaccines. Pediatr Infect Dis J 2002; 21:592.
39. Heiskanen-Kosma T, Korppi M, Leinonen M. Serologically indicated pneumococcal pneumonia in children: a populationbased study in primary care settings. APMIS 2003; 111:945.
40. Korppi M, Heiskanen-Kosma T, Kleemola M. Incidence of community-acquired pneumonia in children caused by
Mycoplasma pneumoniae: serological results of a prospective, population-based study in primary health care. Respirology
2004; 9:109.
41. Kurz H, Gpfrich H, Wabnegger L, Apfalter P. Role of Chlamydophila pneumoniae in children hospitalized for communityacquired pneumonia in Vienna, Austria. Pediatr Pulmonol 2009; 44:873.
42. Carrillo-Marquez MA, Hulten KG, Hammerman W, et al. Staphylococcus aureus pneumonia in children in the era of
community-acquired methicillin-resistance at Texas Children's Hospital. Pediatr Infect Dis J 2011; 30:545.
43. Schwartz KL, Nourse C. Panton-Valentine leukocidin-associated Staphylococcus aureus necrotizing pneumonia in infants:
a report of four cases and review of the literature. Eur J Pediatr 2012; 171:711.
44. Hageman JC, Uyeki TM, Francis JS, et al. Severe community-acquired pneumonia due to Staphylococcus aureus, 200304 influenza season. Emerg Infect Dis 2006; 12:894.
45. Centers for Disease Control and Prevention (CDC). Severe methicillin-resistant Staphylococcus aureus communityacquired pneumonia associated with influenza--Louisiana and Georgia, December 2006-January 2007. MMWR Morb
Mortal Wkly Rep 2007; 56:325.
46. Miller MA, Ben-Ami T, Daum RS. Bacterial pneumonia in neonates and older children. In: Pediatric Respiratory Medicine,
Taussig LM, Landau LI (Eds), Mosby, St. Louis 1999. p.595.
47. Cherry JD, Chen TK. Adenoviruses. In: Textbook of Pediatric Infectious Diseases, 6th, Feigin RD, Cherry JD, DemmlerHarrison GJ, Kaplan SL (Eds), Saunders, Philadelphia 2009. p.1949.
48. Juvn T, Mertsola J, Waris M, et al. Etiology of community-acquired pneumonia in 254 hospitalized children. Pediatr Infect
Dis J 2000; 19:293.
49. McIntosh K. Community-acquired pneumonia in children. N Engl J Med 2002; 346:429.
50. Heugel J, Martin ET, Kuypers J, Englund JA. Coronavirus-associated pneumonia in previously healthy children. Pediatr
Infect Dis J 2007; 26:753.
51. Kahn JS, McIntosh K. History and recent advances in coronavirus discovery. Pediatr Infect Dis J 2005; 24:S223.
52. Longtin J, Bastien M, Gilca R, et al. Human bocavirus infections in hospitalized children and adults. Emerg Infect Dis
2008; 14:217.
53. Abed Y, Boivin G. Human parechovirus types 1, 2 and 3 infections in Canada. Emerg Infect Dis 2006; 12:969.
54. Don M, Sderlund-Venermo M, Valent F, et al. Serologically verified human bocavirus pneumonia in children. Pediatr
Pulmonol 2010; 45:120.
55. Al-Kaabi N, Solh Z, Pacheco S, et al. A Comparison of group A Streptococcus versus Streptococcus pneumoniae
pneumonia. Pediatr Infect Dis J 2006; 25:1008.
56. Esposito S, Bosis S, Cavagna R, et al. Characteristics of Streptococcus pneumoniae and atypical bacterial infections in
children 2-5 years of age with community-acquired pneumonia. Clin Infect Dis 2002; 35:1345.

57. Greenberg D, Chiou CC, Famigilleti R, et al. Problem pathogens: paediatric legionellosis--implications for improved
diagnosis. Lancet Infect Dis 2006; 6:529.
58. Muldoon RL, Jaecker DL, Kiefer HK. Legionnaires' disease in children. Pediatrics 1981; 67:329.
59. Andersen RD, Lauer BA, Fraser DW, et al. Infections with Legionella pneumophila in children. J Infect Dis 1981; 143:386.
60. Stringer JR, Beard CB, Miller RF, Wakefield AE. A new name (Pneumocystis jiroveci) for Pneumocystis from humans.
Emerg Infect Dis 2002; 8:891.
61. De Ceulaer K, McMullen KW, Maude GH, et al. Pneumonia in young children with homozygous sickle cell disease: risk
and clinical features. Eur J Pediatr 1985; 144:255.
Topic 5979 Version 18.0

GRAPHICS Annual all-cause pneumonia hospitalization rates* among children aged

<2 years and 2-4 years - Nationwide Inpatient Sample, United States, 1997-2006

* Per 1000 population. 95% confidence interval. 7-valent pneumococcal conjugate vaccine licensed in February 2000.
Data from: Centers for Disease Control and Prevention. Pneumonia Hospitalizations Among Young Children Before and After
Introduction of Pneumococcal Conjugate Vaccine - United States, 1997-2006. MMWR 2009; 58:3.

Distribution of respiratory viruses obtained from children attending the emergency

department of Milan University's Institute of Pediatrics during the winter season of
2003-2004

Reproduced with permission from: Esposito S, Marchisio P, Principi N. The global state of influenza in children. Pediatr Infect
Dis J 2008; 27:S149. Copyright 2008 Lippincott Williams & Wilkins.

Common etiologic agents of pediatric pneumonia*

Microbial agent

Susceptible hosts

Bacteria

Streptococcus pneumoniae

All

Mycoplasma pneumoniae

Primarily children 5 years

Chlamydophila pneumoniae

Primarily children 5 years

Chlamydia trachomatis

First 3 months of life

Treponema pallidum

First 3 months of life

Mycoplasma hominis

First 3 months of life

Ureaplasma urealyticum

First 3 months of life

Staphylococcus aureus

Primarily children <5 years

Streptococcus pyogenes

Primarily children <5 years

Viruses

Respiratory syncytial virus

Primarily children <5 years

Influenza A and B

Primarily children <5 years

Parainfluenza 1, 2, and 3

Primarily children <5 years

Adenovirus

Primarily children <5 years

Rhinovirus

Primarily children <5 years

Human metapneumovirus

Primarily children <5 years

* Excluding neonatal pneumonia (in infants <28 days of age). Data from: Klein JO, Bacterial pneumonias, In: Textbook of
Pediatric Infectious Diseases, Feigin RD, Cherry JD, Demmler GJ, Kaplan SL (Eds), WB Saunders, Philadelphia 2004,
McIntosh K, N Engl J Med 2002; 346:429, Gaston B, Pediatr Rev 2002; 23:132, Boyer KM. Nonbacterial pneumonia. In:
Textbook of Pediatric Infectious Disease, Feigin BD, Cherry JD, Demmler GJ, Kaplan SL (Eds), WB Saunders, Philadelphia
2004, and Sandora T, Harper MB. Pediatr Clin North Am 2005; 52:1059.

Less common etiologic agents of pediatric pneumonia*

Microbial agent

Susceptible hosts

Bacteria

Haemophilus influenzae (typeable and nontypeable)

Moraxella catarrhalis

Neisseria meningitidis (often group Y)

Klebsiella spp.

Immunocompromised hosts, nosocomial pathogen

Escherichia coli

Immunocompromised hosts, nosocomial pathogen

Enterobacter spp.

Immunocompromised hosts, nosocomial pathogen

Pseudomonas aeruginosa

Immunocompromised hosts, nosocomial pathogen, cystic fibrosis

Burkholderia cepacia

Cystic fibrosis patients

Achromobacter xylosoxidans

Cystic fibrosis patients, nosocomial pathogen

Stenotrophomonas maltophilia

Cystic fibrosis patients, nosocomial pathogen

Legionella pneumophila

Immunocompromised hosts

Pseudomonas pseudomallei

Travelers to or residents of endemic areas

Francisella tularensis

Exposure to a particular animal reservoir (rabbits) or insect vector; bioterrorist

activity

Brucella abortus

Exposure to a particular animal reservoir (cattle, goats)

Chlamydophila psittaci

Exposure to a particular animal reservoir (parakeets)

Leptospira spp.

Exposure to a particular animal reservoir

Yersinia pestis

Exposure to a particular animal reservoir or insect vector (rats); bioterrorist activity

Anaerobic mouth flora (Prevotella spp.,

Fusobacterium, Bacteroides spp.)

Aspiration

Mycobacterium tuberculosis

Travelers to or residents of endemic areas, contact with known TB, homeless,

recent immigrants from endemic areas, prisoners, and HIV-infected individuals

Nontuberculous mycobacterium

Cystic fibrosis patients, immunocompromised hosts

Bordetella pertussis

Infants, exposure to adult with a cough illness

Haemophilus influenzae (typeable and nontypeable)

Moraxella catarrhalis

Neisseria meningitidis (often group Y)

Klebsiella spp.

Immunocompromised hosts, nosocomial pathogen

Escherichia coli

Immunocompromised hosts, nosocomial pathogen

Enterobacter spp.

Immunocompromised hosts, nosocomial pathogen

Pseudomonas aeruginosa

Immunocompromised hosts, nosocomial pathogen, cystic fibrosis

Burkholderia cepacia

Cystic fibrosis patients

Achromobacter xylosoxidans

Cystic fibrosis patients

Stenotrophomonas maltophilia

Cystic fibrosis patients

Legionella pneumophila

Immunocompromised hosts

Pseudomonas pseudomallei

Travelers to or residents of endemic areas

Francisella tularensis

Exposure to a particular animal reservoir (rabbits) or insect vector; bioterrorist

activity

Brucella abortus

Exposure to a particular animal reservoir (cattle, goats)

Chlamydophila psittaci

Exposure to a particular animal reservoir (parakeets)

Leptospira spp.

Exposure to a particular animal reservoir

Yersinia pestis

Exposure to a particular animal reservoir or insect vector (rats); bioterrorist activity

Anaerobic mouth flora (Prevotella spp.,

Fusobacterium, Bacteroides spp.)

Aspiration

Mycobacterium tuberculosis

Travelers to or residents of endemic areas, contact with known TB, homeless,

recent immigrants from endemic areas, prisoners, and HIV-infected individuals

Nontuberculous mycobacterium

Cystic fibrosis patients, immunocompromised hosts

Bordetella pertussis

Infants, exposure to adult with a cough illness

Fungi

Coccidioides immitis

Travelers to or residents of endemic areas (southwest United States)

Histoplasma capsulatum

Travelers to or residents of endemic areas (Ohio and Mississippi River valley)

Blastomyces dermatitidis

Travelers to or residents of endemic areas (Ohio and Mississippi River valley)

Candida spp.

Nosocomial pathogen, immunocompromised hosts, cystic fibrosis

Aspergillus spp.

Nosocomial pathogen, immunocompromised hosts, cystic fibrosis

Pneumocystis jiroveci (formerly carinii)

Immunocompromised hosts

Rickettsiae

Coxiella burnetii

Exposure to a particular animal reservoir (sheep)

Rickettsia rickettsii

Exposure to a particular insect vector

Viruses

Rubeola

Travelers to or residents of endemic areas

Herpes simplex virus

Immunocompromised hosts

Cytomegalovirus

Immunocompromised hosts, first 3 months of life

Epstein Barr virus

Immunocompromised hosts

Varicella zoster virus

Immunocompromised hosts

Coronavirus

Enterovirus

Rubella

Hantavirus

Travelers to or residents of endemic areas, exposure to a particular animal

reservoir (mouse droppings)

Human immunodeficiency virus

Mumps

Bocavirus

Parechovirus

Avian influenza

Exposure to birds; travel to affected area

* Excluding neonatal pneumonia (in infants <28 days of age). Data from: Klein JO, Bacterial pneumonias, In: Textbook of
Pediatric Infectious Diseases, Feigin RD, Cherry JD, Demmler GJ, Kaplan SL (Eds), WB Saunders, Philadelphia 2004,
McIntosh K, N Engl J Med 2002; 346:429, Gaston B, Pediatr Rev 2002; 23:132, Boyer KM. Nonbacterial pneumonia. In:
Textbook of Pediatric Infectious Disease, Feigin BD, Cherry JD, Demmler GJ, Kaplan SL (Eds), WB Saunders, Philadelphia
2004, and Sandora T, Harper MB. Pediatr Clin North Am 2005; 52:1059.

Estimated TB incidence rates, by country, 2009

Reproduced with permission from: World Health Organization. WHO Report 2010: Global Tuberculosis Control.
WHO/HTM/TB/2010.7. Geneva, 2010. Copyright 2010 WHO.
2013 UpToDate, Inc. All rights reserved. |Subscription and License Agreement|Release: 21.1 - C21.12
Licensed to: Inst Chihuahuense de Salud|Support Tag: [1103-189.254.162.24-A17C8A0CD7-494946.14]

Official reprint from UpToDate www.uptodate.com

2013 UpToDate
Print|Back

Clinical features and diagnosis of community-acquired pneumonia in children

Author
William J Barson, MD
Section Editors
Sheldon L Kaplan, MD
George B Mallory, MD
Deputy Editor
Mary M Torchia, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2013. |This topic last updated: ene 24, 2013.
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 39C, 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
[SpO2] <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 higherpitched 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 aureus and 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 >39C and leukocytosis (20,000 white
blood cell [WBC]/microL) and older children (<10 years) with fever >38C, 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 communityacquired 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 [1,8487]. 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 contrastenhanced 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
th

th

the Basics. The Basics patient education pieces are written in plain language, at the 5 to 6 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
th

th

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 to 12 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 >39C, 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.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES

1. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and children
older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious
Diseases Society of America. Clin Infect Dis 2011; 53:e25.
2. Harris M, Clark J, Coote N, et al. British Thoracic Society guidelines for the management of community acquired
pneumonia in children: update 2011. Thorax 2011; 66 Suppl 2:ii1.
3. Murphy CG, van de Pol AC, Harper MB, Bachur RG. Clinical predictors of occult pneumonia in the febrile child. Acad
Emerg Med 2007; 14:243.
4. Margolis P, Gadomski A. The rational clinical examination. Does this infant have pneumonia? JAMA 1998; 279:308.
5. Bachur R, Perry H, Harper MB. Occult pneumonias: empiric chest radiographs in febrile children with leukocytosis. Ann
Emerg Med 1999; 33:166.
6. Bradley JS. Management of community-acquired pediatric pneumonia in an era of increasing antibiotic resistance and
conjugate vaccines. Pediatr Infect Dis J 2002; 21:592.
7. Community acquired pneumonia guideline team, Cincinnati Children's Hospital Medical Center. Evidence-based care
guidelines for medical management of community acquired pneumonia in children 60 days to 17 years of age. Guideline
14. www.cincinnatichildrens.org/svc/alpha/h/health-policy/ev-based/pneumonia.htm (Accessed on September 22, 2011).
8. Jadavji T, Law B, Lebel MH, et al. A practical guide for the diagnosis and treatment of pediatric pneumonia. CMAJ 1997;
156:S703.
9. Pereira JC, Escuder MM. The importance of clinical symptoms and signs in the diagnosis of community-acquired
pneumonia. J Trop Pediatr 1998; 44:18.
10. McIntosh K. Community-acquired pneumonia in children. N Engl J Med 2002; 346:429.

11. Palafox M, Guiscafr H, Reyes H, et al. Diagnostic value of tachypnoea in pneumonia defined radiologically. Arch Dis
Child 2000; 82:41.
12. Mahabee-Gittens EM, Grupp-Phelan J, Brody AS, et al. Identifying children with pneumonia in the emergency department.
Clin Pediatr (Phila) 2005; 44:427.
13. Lynch T, Platt R, Gouin S, et al. Can we predict which children with clinically suspected pneumonia will have the presence
of focal infiltrates on chest radiographs? Pediatrics 2004; 113:e186.
14. Smyth A, Carty H, Hart CA. Clinical predictors of hypoxaemia in children with pneumonia. Ann Trop Paediatr 1998; 18:31.
15. World Health Organization. The management of acute respiratory infections in children. In: Practical guidelines for
outpatient care. World Health Organization, Geneva 1995.
16. Russell G. Community acquired pneumonia. Arch Dis Child 2001; 85:445.
17. Simoes EA, Roark R, Berman S, et al. Respiratory rate: measurement of variability over time and accuracy at different
counting periods. Arch Dis Child 1991; 66:1199.
18. Gadomski AM, Khallaf N, el Ansary S, Black RE. Assessment of respiratory rate and chest indrawing in children with ARI
by primary care physicians in Egypt. Bull World Health Organ 1993; 71:523.
19. Berman S, Simoes EA, Lanata C. Respiratory rate and pneumonia in infancy. Arch Dis Child 1991; 66:81.
20. Gadomski AM, Permutt T, Stanton B. Correcting respiratory rate for the presence of fever. J Clin Epidemiol 1994;
47:1043.
21. Margolis PA, Ferkol TW, Marsocci S, et al. Accuracy of the clinical examination in detecting hypoxemia in infants with
respiratory illness. J Pediatr 1994; 124:552.
22. Heulitt MJ, Ablow RC, Santos CC, et al. Febrile infants less than 3 months old: value of chest radiography. Radiology
1988; 167:135.
23. Harari M, Shann F, Spooner V, et al. Clinical signs of pneumonia in children. Lancet 1991; 338:928.
24. Campbell H, Byass P, Lamont AC, et al. Assessment of clinical criteria for identification of severe acute lower respiratory
tract infections in children. Lancet 1989; 1:297.
25. Broughton RA. Infections due to Mycoplasma pneumoniae in childhood. Pediatr Infect Dis 1986; 5:71.
26. Korppi M, Don M, Valent F, Canciani M. The value of clinical features in differentiating between viral, pneumococcal and
atypical bacterial pneumonia in children. Acta Paediatr 2008; 97:943.
27. Wang K, Gill P, Perera R, et al. Clinical symptoms and signs for the diagnosis of Mycoplasma pneumoniae in children and
adolescents with community-acquired pneumonia. Cochrane Database Syst Rev 2012; 10:CD009175.
28. British Thoracic Society Standards of Care Committee. British Thoracic Society Guidelines for the Management of
Community Acquired Pneumonia in Childhood. Thorax 2002; 57 Suppl 1:i1.
29. Tan TQ, Mason EO Jr, Barson WJ, et al. Clinical characteristics and outcome of children with pneumonia attributable to
penicillin-susceptible and penicillin-nonsusceptible Streptococcus pneumoniae. Pediatrics 1998; 102:1369.
30. Leventhal JM. Clinical predictors of pneumonia as a guide to ordering chest roentgenograms. Clin Pediatr (Phila) 1982;
21:730.
31. Tipple MA, Beem MO, Saxon EM. Clinical characteristics of the afebrile pneumonia associated with Chlamydia
trachomatis infection in infants less than 6 months of age. Pediatrics 1979; 63:192.
32. Turner RB, Lande AE, Chase P, et al. Pneumonia in pediatric outpatients: cause and clinical manifestations. J Pediatr
1987; 111:194.
33. Taylor JA, Del Beccaro M, Done S, Winters W. Establishing clinically relevant standards for tachypnea in febrile children
younger than 2 years. Arch Pediatr Adolesc Med 1995; 149:283.
34. Alario AJ, McCarthy PL, Markowitz R, et al. Usefulness of chest radiographs in children with acute lower respiratory tract
disease. J Pediatr 1987; 111:187.
35. Virkki R, Juven T, Rikalainen H, et al. Differentiation of bacterial and viral pneumonia in children. Thorax 2002; 57:438.
36. Korppi M, Kiekara O, Heiskanen-Kosma T, Soimakallio S. Comparison of radiological findings and microbial aetiology of
childhood pneumonia. Acta Paediatr 1993; 82:360.
37. Bettenay FA, de Campo JF, McCrossin DB. Differentiating bacterial from viral pneumonias in children. Pediatr Radiol
1988; 18:453.
38. Bruns AH, Oosterheert JJ, El Moussaoui R, et al. Pneumonia recovery: discrepancies in perspectives of the radiologist,
physician and patient. J Gen Intern Med 2010; 25:203.
39. Davies HD, Wang EE, Manson D, et al. Reliability of the chest radiograph in the diagnosis of lower respiratory infections
in young children. Pediatr Infect Dis J 1996; 15:600.
40. Kramer MS, Roberts-Bruer R, Williams RL. Bias and 'overcall' in interpreting chest radiographs in young febrile children.
Pediatrics 1992; 90:11.
41. Swingler GH, Hussey GD, Zwarenstein M. Randomised controlled trial of clinical outcome after chest radiograph in
ambulatory acute lower-respiratory infection in children. Lancet 1998; 351:404.
42. Ablin DS, Newell JD 2nd. Diagnostic imaging for evaluation of the pediatric chest. Clin Chest Med 1987; 8:641.
43. Gaisie G, Dominguez R, Young LW. Comparison of AP supine vs PA upright methods of chest roentgenography in infants
and young children. J Natl Med Assoc 1984; 76:171.
44. Miller MA, Ben-Ami T, Daum RS. Bacterial pneumonia in neonates and older children. In: Pediatric Respiratory Medicine,
Taussig LM, Landau LI (Eds), Mosby, St. Louis 1999. p.595.
45. Kiekara O, Korppi M, Tanska S, Soimakallio S. Radiological diagnosis of pneumonia in children. Ann Med 1996; 28:69.

46. Kuhn JP, Brody AS. High-resolution CT of pediatric lung disease. Radiol Clin North Am 2002; 40:89.
47. Courtoy I, Lande AE, Turner RB. Accuracy of radiographic differentiation of bacterial from nonbacterial pneumonia. Clin
Pediatr (Phila) 1989; 28:261.
48. McCarthy PL, Spiesel SZ, Stashwick CA, et al. Radiographic findings and etiologic diagnosis in ambulatory childhood
pneumonias. Clin Pediatr (Phila) 1981; 20:686.
49. Clements H, Stephenson T, Gabriel V, et al. Rationalised prescribing for community acquired pneumonia: a closed loop
audit. Arch Dis Child 2000; 83:320.
50. Lahti E, Peltola V, Virkki R, Ruuskanen O. Influenza pneumonia. Pediatr Infect Dis J 2006; 25:160.
51. Simpson W, Hacking PM, Court SD, Gardner PS. The radiological findings in respiratory syncytial virus infection in
children. II. The correlation of radiological categories with clinical and virological findings. Pediatr Radiol 1974; 2:155.
52. Dawson KP, Long A, Kennedy J, Mogridge N. The chest radiograph in acute bronchiolitis. J Paediatr Child Health 1990;
26:209.
53. Finnegan OC, Fowles SJ, White RJ. Radiographic appearances of mycoplasma pneumonia. Thorax 1981; 36:469.
54. Griscom NT. Pneumonia in children and some of its variants. Radiology 1988; 167:297.
55. McLennan MK. Radiology rounds. Round pneumonia. Can Fam Physician 1998; 44:751, 757.
56. Kim YW, Donnelly LF. Round pneumonia: imaging findings in a large series of children. Pediatr Radiol 2007; 37:1235.
57. Redd SC, Patrick E, Vreuls R, et al. Comparison of the clinical and radiographic diagnosis of paediatric pneumonia. Trans
R Soc Trop Med Hyg 1994; 88:307.
58. Shuttleworth DB, Charney E. Leukocyte count in childhood pneumonia. Am J Dis Child 1971; 122:393.
59. Peltola V, Mertsola J, Ruuskanen O. Comparison of total white blood cell count and serum C-reactive protein levels in
confirmed bacterial and viral infections. J Pediatr 2006; 149:721.
60. Tabain I, Ljubin-Sternak S, Cepin-Bogovi J, et al. Adenovirus respiratory infections in hospitalized children: clinical
findings in relation to species and serotypes. Pediatr Infect Dis J 2012; 31:680.
61. Chen SP, Huang YC, Chiu CH, et al. Clinical features of radiologically confirmed pneumonia due to adenovirus in
children. J Clin Virol 2013; 56:7.
62. Flood RG, Badik J, Aronoff SC. The utility of serum C-reactive protein in differentiating bacterial from nonbacterial
pneumonia in children: a meta-analysis of 1230 children. Pediatr Infect Dis J 2008; 27:95.
63. Moulin F, Raymond J, Lorrot M, et al. Procalcitonin in children admitted to hospital with community acquired pneumonia.
Arch Dis Child 2001; 84:332.
64. Schtzle H, Forster J, Superti-Furga A, Berner R. Is serum procalcitonin a reliable diagnostic marker in children with acute
respiratory tract infections? A retrospective analysis. Eur J Pediatr 2009; 168:1117.
65. Toikka P, Irjala K, Juvn T, et al. Serum procalcitonin, C-reactive protein and interleukin-6 for distinguishing bacterial and
viral pneumonia in children. Pediatr Infect Dis J 2000; 19:598.
66. van Rossum AM, Wulkan RW, Oudesluys-Murphy AM. Procalcitonin as an early marker of infection in neonates and
children. Lancet Infect Dis 2004; 4:620.
67. Korppi M. Non-specific host response markers in the differentiation between pneumococcal and viral pneumonia: what is
the most accurate combination? Pediatr Int 2004; 46:545.
68. Korppi M, Remes S, Heiskanen-Kosma T. Serum procalcitonin concentrations in bacterial pneumonia in children: a
negative result in primary healthcare settings. Pediatr Pulmonol 2003; 35:56.
69. Ostapchuk M, Roberts DM, Haddy R. Community-acquired pneumonia in infants and children. Am Fam Physician 2004;
70:899.
70. McCracken GH Jr. Diagnosis and management of pneumonia in children. Pediatr Infect Dis J 2000; 19:924.
71. Sandora TJ, Harper MB. Pneumonia in hospitalized children. Pediatr Clin North Am 2005; 52:1059.
72. Hickey RW, Bowman MJ, Smith GA. Utility of blood cultures in pediatric patients found to have pneumonia in the
emergency department. Ann Emerg Med 1996; 27:721.
73. Shah SS, Dugan MH, Bell LM, et al. Blood cultures in the emergency department evaluation of childhood pneumonia.
Pediatr Infect Dis J 2011; 30:475.
74. Byington CL, Spencer LY, Johnson TA, et al. An epidemiological investigation of a sustained high rate of pediatric
parapneumonic empyema: risk factors and microbiological associations. Clin Infect Dis 2002; 34:434.
75. Byington CL, Korgenski K, Daly J, et al. Impact of the pneumococcal conjugate vaccine on pneumococcal parapneumonic
empyema. Pediatr Infect Dis J 2006; 25:250.
76. St Peter SD, Tsao K, Spilde TL, et al. Thoracoscopic decortication vs tube thoracostomy with fibrinolysis for empyema in
children: a prospective, randomized trial. J Pediatr Surg 2009; 44:106.
77. Claesson BA, Trollfors B, Brolin I, et al. Etiology of community-acquired pneumonia in children based on antibody
responses to bacterial and viral antigens. Pediatr Infect Dis J 1989; 8:856.
78. Lahti E, Peltola V, Waris M, et al. Induced sputum in the diagnosis of childhood community-acquired pneumonia. Thorax
2009; 64:252.
79. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society
consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007; 44 Suppl
2:S27.
80. Murray PR, Washington JA. Microscopic and baceriologic analysis of expectorated sputum. Mayo Clin Proc 1975; 50:339.

81. Rein MF, Gwaltney JM Jr, O'Brien WM, et al. Accuracy of Gram's stain in identifying pneumococci in sputum. JAMA 1978;
239:2671.
82. Honda J, Yano T, Kusaba M, et al. Clinical use of capillary PCR to diagnose Mycoplasma pneumonia. J Clin Microbiol
2000; 38:1382.
83. Skerrett SJ. Diagnostic testing for community-acquired pneumonia. Clin Chest Med 1999; 20:531.
84. Vuori-Holopainen E, Salo E, Saxn H, et al. Etiological diagnosis of childhood pneumonia by use of transthoracic needle
aspiration and modern microbiological methods. Clin Infect Dis 2002; 34:583.
85. Kornecki A, Shemie SD. Open lung biopsy in children with respiratory failure. Crit Care Med 2001; 29:1247.
86. Hayes-Jordan A, Benaim E, Richardson S, et al. Open lung biopsy in pediatric bone marrow transplant patients. J Pediatr
Surg 2002; 37:446.
87. De Schutter I, De Wachter E, Crokaert F, et al. Microbiology of bronchoalveolar lavage fluid in children with acute
nonresponding or recurrent community-acquired pneumonia: identification of nontypeable Haemophilus influenzae as a
major pathogen. Clin Infect Dis 2011; 52:1437.
88. Loens K, Van Heirstraeten L, Malhotra-Kumar S, et al. Optimal sampling sites and methods for detection of pathogens
possibly causing community-acquired lower respiratory tract infections. J Clin Microbiol 2009; 47:21.
89. de Blic J, Midulla F, Barbato A, et al. Bronchoalveolar lavage in children. ERS Task Force on bronchoalveolar lavage in
children. European Respiratory Society. Eur Respir J 2000; 15:217.
90. Kirkpatrick MB, Bass JB Jr. Quantitative bacterial cultures of bronchoalveolar lavage fluids and protected brush catheter
specimens from normal subjects. Am Rev Respir Dis 1989; 139:546.
91. Naiditch JA, Barsness KA, Rothstein DH. The utility of surgical lung biopsy in immunocompromised children. J Pediatr
2013; 162:133.
92. Crain EF, Bulas D, Bijur PE, Goldman HS. Is a chest radiograph necessary in the evaluation of every febrile infant less
than 8 weeks of age? Pediatrics 1991; 88:821.
93. Wingerter SL, Bachur RG, Monuteaux MC, Neuman MI. Application of the world health organization criteria to predict
radiographic pneumonia in a US-based pediatric emergency department. Pediatr Infect Dis J 2012; 31:561.
94. Mani CS, Murray DL. Acute pneumonia and its complications. In: Principles and Practice of Pediatric Infectious Diseases,
4th, Long SS, Pickering LK, Prober CG. (Eds), Elsevier Saunders, Edinburgh 2012. p.235.
95. Gaston B. Pneumonia. Pediatr Rev 2002; 23:132.
96. Clark CE, Coote JM, Silver DA, Halpin DM. Asthma after childhood pneumonia: six year follow up study. BMJ 2000;
320:1514.
97. Chen KC, Su YT, Lin WL, et al. Clinical analysis of necrotizing pneumonia in children: three-year experience in a single
medical center. Acta Paediatr Taiwan 2003; 44:343.
98. Kerem E, Bar Ziv Y, Rudenski B, et al. Bacteremic necrotizing pneumococcal pneumonia in children. Am J Respir Crit
Care Med 1994; 149:242.
99. McCarthy VP, Patamasucon P, Gaines T, Lucas MA. Necrotizing pneumococcal pneumonia in childhood. Pediatr
Pulmonol 1999; 28:217.
100.
Ramphul N, Eastham KM, Freeman R, et al. Cavitatory lung disease complicating empyema in children. Pediatr
Pulmonol 2006; 41:750.
101.
Bender JM, Ampofo K, Korgenski K, et al. Pneumococcal necrotizing pneumonia in Utah: does serotype matter?
Clin Infect Dis 2008; 46:1346.
102.
Sawicki GS, Lu FL, Valim C, et al. Necrotising pneumonia is an increasingly detected complication of pneumonia
in children. Eur Respir J 2008; 31:1285.
103.
Cengiz AB, Kanra G, Calar M, et al. Fatal necrotizing pneumonia caused by group A streptococcus. J Paediatr
Child Health 2004; 40:69.
104.
Wang RS, Wang SY, Hsieh KS, et al. Necrotizing pneumonitis caused by Mycoplasma pneumoniae in pediatric
patients: report of five cases and review of literature. Pediatr Infect Dis J 2004; 23:564.
105.
Hodina M, Hanquinet S, Cotting J, et al. Imaging of cavitary necrosis in complicated childhood pneumonia. Eur
Radiol 2002; 12:391.
106.
Schwartz KL, Nourse C. Panton-Valentine leukocidin-associated Staphylococcus aureus necrotizing pneumonia
in infants: a report of four cases and review of the literature. Eur J Pediatr 2012; 171:711.
107.
Groskin SA, Panicek DM, Ewing DK, et al. Bacterial lung abscess: a review of the radiographic and clinical
features of 50 cases. J Thorac Imaging 1991; 6:62.
108.
Emanuel B, Shulman ST. Lung abscess in infants and children. Clin Pediatr (Phila) 1995; 34:2.
109.
Donnelly LF, Klosterman LA. The yield of CT of children who have complicated pneumonia and noncontributory
chest radiography. AJR Am J Roentgenol 1998; 170:1627.
110.
Tan TQ, Seilheimer DK, Kaplan SL. Pediatric lung abscess: clinical management and outcome. Pediatr Infect Dis
J 1995; 14:51.
111.
Lorber B. "Bad breath": presenting manifestation of anaerobic pulmonary infection. Am Rev Respir Dis 1975;
112:875.
112.
Brook I. Lung abscesses and pleural empyema in children. Adv Pediatr Infect Dis 1993; 8:159.
113.
Brook I, Finegold SM. Bacteriology and therapy of lung abscess in children. J Pediatr 1979; 94:10.

114.
Hacimustafaoglu M, Celebi S, Sarimehmet H, et al. Necrotizing pneumonia in children. Acta Paediatr 2004;
93:1172.
115.
Johnson JF, Shiels WE, White CB, Williams BD. Concealed pulmonary abscess: diagnosis by computed
tomography. Pediatrics 1986; 78:283.
116.
Kunyoshi V, Cataneo DC, Cataneo AJ. Complicated pneumonias with empyema and/or pneumatocele in children.
Pediatr Surg Int 2006; 22:186.
117.
Amitai I, Mogle P, Godfrey S, Aviad I. Pneumatocele in infants and children. Report of 12 cases. Clin Pediatr
(Phila) 1983; 22:420.
118.
Ceruti E, Contreras J, Neira M. Staphylococcal pneumonia in childhood. Long-term follow-up including pulmonary
function studies. Am J Dis Child 1971; 122:386.
119.
Soto M, Demis T, Landau LI. Pulmonary function following staphylococcal pneumonia in children. Aust Paediatr J
1983; 19:172.
120.
Singhi S, Dhawan A. Frequency and significance of electrolyte abnormalities in pneumonia. Indian Pediatr 1992;
29:735.
121.
Dhawan A, Narang A, Singhi S. Hyponatraemia and the inappropriate ADH syndrome in pneumonia. Ann Trop
Paediatr 1992; 12:455.
122.
Don M, Valerio G, Korppi M, Canciani M. Hyponatremia in pediatric community-acquired pneumonia. Pediatr
Nephrol 2008; 23:2247.
Topic 5986 Version 20.0

GRAPHICS Important aspects of the history in a child with pneumonia

Historical feature
Age of the child

Possible significance

Viral etiologies are most common in infants and preschool children

Atypical bacterial pathogens are more common in school-age children

Recent viral upper respiratory tract

infection

May predispose to bacterial superinfection with Streptococcus pneumoniae or

Staphylococcus aureus

Associated symptoms

Mycoplasma pneumoniae is often associated with extrapulmonary manifestations (eg,

headache, photophobia, rash)

Presence of cough, chest pain,

shortness of breath, difficulty
breathing

"Classic" features of pneumonia, but non-specific

Increased work of breathing in the

absence of stridor or wheezing

Suggestive of severe pneumonia

Choking episode

May indicate foreign body aspiration

Duration of symptoms

Chronic cough (>4 weeks) suggests etiology other than acute pneumonia (refer to UpToDate
topic on causes of chronic cough in children)

Previous episodes

Recurrent episodes may indicate aspiration, congenital or acquired anatomic abnormality,

cystic fibrosis, immunodeficiency, asthma, missed foreign body

Immunization status

Completion of the primary series of immunizations for Haemophilus influenzae type b,

Streptococcus pneumoniae, Bordetella pertussis, and seasonal influenza decreases, but
does not eliminate, the risk of infection with these organisms

Previous antibiotic therapy

Increases the likelihood of antibiotic-resistant bacteria

Maternal history of chlamydia

during pregnancy (for infants <4
months of age)

May indicate Chlamydia trachomatis infection

Exposure to tuberculosis

May indicate Mycobacterium tuberculosis infection

Ill contacts

More common with viral etiologies

Travel to or residence in certain

areas that suggest endemic
pathogens

Measles: Developing world

Coccidioidomycosis: Southwestern US, northern Mexico, Central and South America
Blastomycosis: Southeastern and central US; states bordering the Great Lakes
Histoplasmosis: Ohio, Missouri, and Mississippi River valleys in the United States; Canada;
Central America; eastern and southern Europe; parts of Africa; eastern Asia; and Australia
Hantavirus: West of the Mississippi River; four corners region of United States (where
borders of Colorado, New Mexico, Arizona, and Utah meet)

Animal exposure

May indicate histoplasmosis, psittacosis, Q fever

Day care center attendance

Exposure to viruses and antibiotic-resistant bacteria

Fluid and nutrition intake

Difficulty or inability to feed suggests severe illness

Important aspects of the physical examination in a child with suspected

pneumonia
Examination feature
General appearance (state of
awareness, cyanosis)*

Possible significance
Most children with radiographically confirmed pneumonia appear ill

Vital signs

Temperature

Respiratory rate

Fever may be the only sign of pneumonia in highly febrile young children; however, it is
variably present and nonspecific

Tachypnea correlates with radiographically confirmed pneumonia and hypoxemia

Absence of tachypnea helps to exclude pneumonia

Degree of respiratory distress

Respiratory distress is more specific than fever or cough for lower respiratory infection

Tachypnea

Hypoxemia

Predictive of pneumonia

Increased work of breathing:

Retractions

More common in children with pneumonia than without; absence does not exclude pneumonia

Nasal flaring

More common in children with pneumonia than without; absence does not exclude pneumonia

Grunting

Sign of severe disease and pending respiratory failure

Accessory muscle use

Sign of severe disease

Head bobbing

Sign of severe disease

Lung examination

Cough

Auscultation

Nonspecific finding of pneumonia

Findings suggestive of pneumonia include: crackles (rales, crepitations), decreased breath

sounds, bronchial breath sounds, egophany, bronchophony, and whispered pectoriloquy
Wheezing more common in viral and atypical pneumonias

Tactile fremitus

Suggestive of parenchymal consolidation

Dullness to percussion

Suggestive of parenchymal consolidation or pleural effusion

Mental status

Altered mental status may be a sign of hypoxia

* For young infants: Ability to attend to the environment, feed, vocalize, and be consoled. World Health Organization
definitions of tachypnea according to age are as follows: <2 months: >60 breaths/min; 2 to 12 months: >50 breaths/min; 1
to 5 years: >40 breaths/min; 5 years: >20 breaths/min.

Severity of community acquired pneumonia in infants and children

Clinical features of mild pneumonia

Clinical features of severe pneumonia

Temperature <38.5C (101.3F)

Temperature 38.5C (101.3F)

Mild or absent respiratory distress:

Moderate to severe respiratory distress:

Increased RR, but less than the age-specific RR that defines

moderate to severe respiratory distress

RR >70 breaths/minute for infants; RR >50 breaths/minute

for older children

Mild or absent retractions

No grunting

Moderate/severe suprasternal, intercostal, or subcostal

retractions (<12 months)

No nasal flaring

Severe difficulty breathing (12 months)

No apnea

Grunting

Mild shortness of breath

Nasal flaring

Apnea

Significant shortness of breath

Normal color

Cyanosis

Normal mental status

Altered mental status

Normoxemia (oxygen saturation 92 percent in room air)

Hypoxemia (sustained oxygen saturation <90 percent in

room air at sea level)

Normal feeding (infants); no vomiting

Not feeding (infants) or signs of dehydration (older children)

Normal heart rate

Tachycardia

Capillary refill <2 seconds

Capillary refill 2 seconds

RR: respiratory rate. Data from: Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired
pneumonia in infants and children older than 3 months of age: Clinical practice guidelines by the Pediatric Infectious Diseases
Society and the Infectious Diseases Society of America. Clin Infect Dis 2011; 53:e25. Harris M, Clark J, Coote N, et al. British
Thoracic Society guidelines for the management of community acquired pneumonia in children: update 2011. Thorax 2011;
66:ii1.

Clinical and radiographic clues to the etiology of pneumonia in children*

Etiology

Bacteria(most commonly Streptococcus

pneumoniae)

Atypical bacterial(Mycoplasma
pneumoniae, Chlamydophila
pneumoniae)

Radiographic
features

Clinical features

Children of all ages

Alveolar infiltrates

Abrupt onset

Segmental consolidation

Ill-appearance

Lobar consolidation

Chills

"Round" pneumonia

Moderate to severe respiratory distress

Focal auscultatory findings

Localized chest pain

WBC count >15,000/microL (if obtained)

Elevated acute phase reactants (if obtained)

Complications:

Pleural
effusion/empyema

Lung abscess

Necrotizing pneumonia

Pneumatocele
Interstitial infiltrates

Children of all ages (most common in children >5 years)

Abrupt onset with constitutional findings (malaise, myalgia,

headache, conjunctivitis, photophobia, sore throat,
headache)

Gradually worsening nonproductive cough

Wheezing

Extrapulmonary manifestations or complications (eg,

Stevens-Johnson syndrome, hemolytic anemia, hepatitis,
etc)

Usually children <5 years

Gradual onset

Preceding upper airway symptoms

Non-toxic appearing

Diffuse, bilateral auscultatory findings

Wheezing

May have associated rash (eg, measles, varicella)

Usually in infants 2 weeks to 4 months

Insidious onset

Rhinorrhea

Staccato cough pattern

Peripheral eosinophilia (if CBC obtained)

Fungal

Appropriate geographic or environmental exposure

Mediastinal or hilar
adenopathy

Mycobacterium tuberculosis

Children of any age

Mediastinal or hilar
adenopathy

Chronic cough

Constitutional symptoms

Exposure history

Viral

Afebrile pneumonia of infancy (most

commonly Chlamydia trachomatis)

Interstitial infiltrates

Hyperinflation with
interstitial process

WBC: white blood cell; CBC: complete blood count. * The clinical features frequently overlap and cannot reliably distinguish
between bacterial, atypical bacterial, and viral etiologies; up to one-half of community-acquired pneumonias in children may
be mixed bacterial/viral infections. Chest radiography generally is not helpful in determining the potential causative agent of
pneumonia. Nonetheless, these features may facilitate decisions regarding empiric therapy. Data from: Bartlett JG, Mundy
LM. Community-acquired pneumonia. N Engl J Med 1995; 333:1618. Boyer KM. Nonbacterial pneumonia. In: Textbook of
Pediatric Infectious Diseases, 6th ed, Feigin RD, Cherry JD, Demmler-Harrison GJ, Kaplan SL (Eds), Saunders, Philadelphia
2009. p.289. Broughton RA. Infections due to Mycoplasma pneumoniae in childhood. Pediatr Infect Dis 1986; 5:71. McIntosh
K. Community-acquired pneumonia in children. N Engl J Med 2002; 346:429.

Boy with measles

Source: Centers for Disease Control and Prevention.

Measles exanthem

Blanching erythematous rash with some confluent areas on the trunk in a patient with measles. Copyright
Dr. Michael Bennish; reproduced with his permission.

Primary varicella lesions

Vesicular lesions on an erythematous base are characteristic of chickenpox. The lesions occur in crops and
are present in a variety of stages from maculopapular to vesicular or even pustular. Central necrosis and
early crusting is also visible. Courtesy of Lee T Nesbitt, Jr. The Skin and Infection: A Color Atlas and Text, Sanders CV,
Nesbitt LT Jr (Eds), Williams & Wilkins, Baltimore 1995. http://www.lww.com

Herpes simplex virus infection of the hand

Close-up view of vesicles on an erythematous base. Courtesy of Beth G Goldstein, MD and Adam O Goldstein, MD.

Herpes simplex labialis

Grouped vesicles are evident on the lower vermilion border. Reproduced with permission from: Bickley LS, Szilagyi
P. Bates' Guide to Physical Examination and History Taking, Eighth Edition. Philadelphia: Lippincott Williams & Wilkins, 2003.
Copyright 2003 Lippincott Williams & Wilkins.

Right-sided pneumonia with pleural effusion

Courtesy of Dwight A Powell, MD.

Computed tomography: Left-sided pneumonia with pleural effusion

Courtesy of Dwight A Powell, MD.

Computed tomography: Left-sided Streptococcus pneumoniae necrotizing

pneumonia

Courtesy William J Barson, MD.

Plain radiograph: Mycoplasma pneumoniae pneumonia

Diffuse bilateral interstitial infiltrates with M. pneumoniae infection. Courtesy of Dwight A Powell, MD.

Sputum from a patient with pneumococcal pneumonia

Gram stain of sputum (x1000) shows abundant inflammatory cells and gram-positive diplococci;
Streptococcus pneumoniae was identified from this specimen by culture and by the optochin disk test.
Courtesy of Harriet Provine.

Noninfectious condititions that can mimic pneumonia in children

Anatomical considerations

Drugs and chemical exposures

Prominent thymus

Nitrofurantoin

Breast shadows

Bleomycin

Bronchogenic cyst

Cytotoxic drugs

Vascular ring

Opiates

Pulmonary sequestration

Radiation therapy

Congenital lobar emphysema

Smoke inhalation

Atelectasis (due to a foreign body or mucus plug)

Lipoid pneumonia

Aspiration of gastric contents

Vasculitic disorders

Gastroesophageal reflux

Systemic lupus erythematosus

Tracheoesophageal fistula

Granulomatosis with polyangiitis (Wegener's)

Cleft palate

Juvenile idiopathic arthritis

Neuromuscular disorders

Others

Chronic pulmonary disorders

Hypersensitivity pneumonitis

Asthma

Neoplasm

Bronchiectasis

Pulmonary edema due to heart failure

Bronchopulmonary dysplasia

Pulmonary infarction

Cystic fibrosis

Acute respiratory distress syndrome

Pulmonary fibrosis

Graft-versus-host disease

Alpha1-antitrypsin deficiency

Poor inspiratory film

Pulmonary hemosiderosis

Near drowning event

Alveolar proteinosis

Underpenetrated film

Desquamative interstitial pneumonitis

Sarcoidosis
Histiocytosis X

Data from: Klein JO. Bacterial pneumonias. In: Textbook of Pediatric Infectious Diseases, 5th ed, Feigin RD, Cherry JD,
Demmler GJ, Kaplan SL (Eds), WB Saunders, Philadelphia 2004. p.299. McIntosh K. Community-acquired pneumonia in
children. N Engl J Med 2002; 346:429. Gaston B. Pneumonia. Pediatr Rev 2002; 23:132. Boyer KM. Nonbacterial pneumonia.
In: Textbook of Pediatric Infectious Disease, 5th ed, Feigin RD, Cherry JD, Demmler GJ, Kaplan SL (Eds), WB Saunders,
Philadelphia 2004. p.286.

Complications of pneumococcal pneumonia

Radiographic images of the complications of pneumococcal pneumonia. (Left panel) Lung abscess with an
air-fluid level in the right lung. Abscess cavity material is nearly always culture positive, and patients
commonly defervesce within 48 hours of interventional drainage. (Right panel) Radiograph of necrotizing
pneumonia in the left lung.
2013 UpToDate, Inc. All rights reserved. |Subscription and License Agreement|Release: 21.1 - C21.12
Licensed to: Inst Chihuahuense de Salud|Support Tag: [1103-189.254.162.24-A17C8A0CD7-494946.14]

Official reprint from UpToDate www.uptodate.com

2013 UpToDate
Print|Back

Outpatient treatment of community-acquired pneumonia in children

Author
William J Barson, MD
Section Editors
Morven S Edwards, MD
George B Mallory, MD
Deputy Editor
Mary M Torchia, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2013. |This topic last updated: dic 20, 2012.
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. pertussis is 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 6 mg/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 communityacquired 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 penicillinresistant S. pneumoniae is suspected, a change in antibiotic therapy to clindamycin 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-dose amoxicillin, 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
th

th

the Basics. The Basics patient education pieces are written in plain language, at the 5 to 6 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
th

th

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 to 12 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.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES

1. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and children
older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious
Diseases Society of America. Clin Infect Dis 2011; 53:e25.
2. Harris M, Clark J, Coote N, et al. British Thoracic Society guidelines for the management of community acquired
pneumonia in children: update 2011. Thorax 2011; 66 Suppl 2:ii1.
3. Russell G. Community acquired pneumonia. Arch Dis Child 2001; 85:445.
4. McIntosh K. Community-acquired pneumonia in children. N Engl J Med 2002; 346:429.
5. Esposito S, Bosis S, Cavagna R, et al. Characteristics of Streptococcus pneumoniae and atypical bacterial infections in
children 2-5 years of age with community-acquired pneumonia. Clin Infect Dis 2002; 35:1345.
6. Virkki R, Juven T, Rikalainen H, et al. Differentiation of bacterial and viral pneumonia in children. Thorax 2002; 57:438.
7. Low DE, Pichichero ME, Schaad UB. Optimizing antibacterial therapy for community-acquired respiratory tract infections
in children in an era of bacterial resistance. Clin Pediatr (Phila) 2004; 43:135.
8. Harris JA, Kolokathis A, Campbell M, et al. Safety and efficacy of azithromycin in the treatment of community-acquired
pneumonia in children. Pediatr Infect Dis J 1998; 17:865.
9. Wubbel L, Muniz L, Ahmed A, et al. Etiology and treatment of community-acquired pneumonia in ambulatory children.
Pediatr Infect Dis J 1999; 18:98.
10. Jadavji T, Law B, Lebel MH, et al. A practical guide for the diagnosis and treatment of pediatric pneumonia. CMAJ 1997;
156:S703.
11. Gordon KA, Biedenbach DJ, Jones RN. Comparison of Streptococcus pneumoniae and Haemophilus influenzae
susceptibilities from community-acquired respiratory tract infections and hospitalized patients with pneumonia: five-year
results for the SENTRY Antimicrobial Surveillance Program. Diagn Microbiol Infect Dis 2003; 46:285.
12. Hyde TB, Gay K, Stephens DS, et al. Macrolide resistance among invasive Streptococcus pneumoniae isolates. JAMA
2001; 286:1857.
13. Hoberman A, Paradise JL, Burch DJ, et al. Equivalent efficacy and reduced occurrence of diarrhea from a new
formulation of amoxicillin/clavulanate potassium (Augmentin) for treatment of acute otitis media in children. Pediatr Infect
Dis J 1997; 16:463.
14. Behre U, Burow HM, Quinn P, et al. Efficacy of twice-daily dosing of amoxycillin/clavulanate in acute otitis media in
children. Infection 1997; 25:163.
15. Principi N, Marchisio P, Bigalli L, Massironi E. Amoxicillin twice daily in the treatment of acute otitis media in infants and
children. Eur J Pediatr 1986; 145:522.
16. Bradley JS, Garonzik SM, Forrest A, Bhavnani SM. Pharmacokinetics, pharmacodynamics, and Monte Carlo simulation:
selecting the best antimicrobial dose to treat an infection. Pediatr Infect Dis J 2010; 29:1043.

17. Baskin MN, O'Rourke EJ, Fleisher GR. Outpatient treatment of febrile infants 28 to 89 days of age with intramuscular
administration of ceftriaxone. J Pediatr 1992; 120:22.
18. Chumpa A, Bachur RG, Harper MB. Bacteremia-associated pneumococcal pneumonia and the benefit of initial parenteral
antimicrobial therapy. Pediatr Infect Dis J 1999; 18:1081.
19. Hammerschlag MR. Atypical pneumonias in children. Adv Pediatr Infect Dis 1995; 10:1.
20. Peuchant O, Mnard A, Renaudin H, et al. Increased macrolide resistance of Mycoplasma pneumoniae in France directly
detected in clinical specimens by real-time PCR and melting curve analysis. J Antimicrob Chemother 2009; 64:52.
21. Averbuch D, Hidalgo-Grass C, Moses AE, et al. Macrolide resistance in Mycoplasma pneumoniae, Israel, 2010. Emerg
Infect Dis 2011; 17:1079.
22. Yamada M, Buller R, Bledsoe S, Storch GA. Rising rates of macrolide-resistant Mycoplasma pneumoniae in the central
United States. Pediatr Infect Dis J 2012; 31:409.
23. Kawai Y, Miyashita N, Yamaguchi T, et al. Clinical efficacy of macrolide antibiotics against genetically determined
macrolide-resistant Mycoplasma pneumoniae pneumonia in paediatric patients. Respirology 2012; 17:354.
24. Chironna M, Sallustio A, Esposito S, et al. Emergence of macrolide-resistant strains during an outbreak of Mycoplasma
pneumoniae infections in children. J Antimicrob Chemother 2011; 66:734.
25. Liu Y, Ye X, Zhang H, et al. Characterization of macrolide resistance in Mycoplasma pneumoniae isolated from children in
Shanghai, China. Diagn Microbiol Infect Dis 2010; 67:355.
26. Miyashita N, Kawai Y, Akaike H, et al. Macrolide-resistant Mycoplasma pneumoniae in adolescents with communityacquired pneumonia. BMC Infect Dis 2012; 12:126.
27. Centers for Disease Control and Prevention (CDC). Mycoplasma pneumoniae respiratory illness - two rural counties,
West Virginia, 2011. MMWR Morb Mortal Wkly Rep 2012; 61:834.
28. Block S, Hedrick J, Hammerschlag MR, et al. Mycoplasma pneumoniae and Chlamydia pneumoniae in pediatric
community-acquired pneumonia: comparative efficacy and safety of clarithromycin vs. erythromycin ethylsuccinate.
Pediatr Infect Dis J 1995; 14:471.
29. Chien SM, Pichotta P, Siepman N, Chan CK. Treatment of community-acquired pneumonia. A multicenter, double-blind,
randomized study comparing clarithromycin with erythromycin. Canada-Sweden Clarithromycin-Pneumonia Study Group.
Chest 1993; 103:697.
30. Pelton SI, Hammerschlag MR. Overcoming current obstacles in the management of bacterial community-acquired
pneumonia in ambulatory children. Clin Pediatr (Phila) 2005; 44:1.
31. Bartlett JG, Mundy LM. Community-acquired pneumonia. N Engl J Med 1995; 333:1618.
32. Sandora TJ, Harper MB. Pneumonia in hospitalized children. Pediatr Clin North Am 2005; 52:1059.
33. Bradley JS, Arguedas A, Blumer JL, et al. Comparative study of levofloxacin in the treatment of children with communityacquired pneumonia. Pediatr Infect Dis J 2007; 26:868.
34. Davidson R, Cavalcanti R, Brunton JL, et al. Resistance to levofloxacin and failure of treatment of pneumococcal
pneumonia. N Engl J Med 2002; 346:747.
35. Haider BA, Saeed MA, Bhutta ZA. Short-course versus long-course antibiotic therapy for non-severe community-acquired
pneumonia in children aged 2 months to 59 months. Cochrane Database Syst Rev 2008; :CD005976.
36. Hazir T, Nisar YB, Qazi SA, et al. Chest radiography in children aged 2-59 months diagnosed with non-severe pneumonia
as defined by World Health Organization: descriptive multicentre study in Pakistan. BMJ 2006; 333:629.
37. Hazir T, Nisar YB, Abbasi S, et al. Comparison of oral amoxicillin with placebo for the treatment of world health
organization-defined nonsevere pneumonia in children aged 2-59 months: a multicenter, double-blind, randomized,
placebo-controlled trial in pakistan. Clin Infect Dis 2011; 52:293.
38. Alves dos Santos JW, Torres A, Michel GT, et al. Non-infectious and unusual infectious mimics of community-acquired
pneumonia. Respir Med 2004; 98:488.
39. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the
treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52:e18.
40. Bbar C, Pereyre S, Peuchant O. Mycoplasma pneumoniae: susceptibility and resistance to antibiotics. Future Microbiol
2011; 6:423.
41. Gaston B. Pneumonia. Pediatr Rev 2002; 23:132.
42. Griscom NT. Pneumonia in children and some of its variants. Radiology 1988; 167:297.
43. McLennan MK. Radiology rounds. Round pneumonia. Can Fam Physician 1998; 44:751, 757.
44. Kim YW, Donnelly LF. Round pneumonia: imaging findings in a large series of children. Pediatr Radiol 2007; 37:1235.
45. Eggli KD, Newman B. Nodules, masses, and pseudomasses in the pediatric lung. Radiol Clin North Am 1993; 31:651.
46. Rose RW, Ward BH. Spherical pneumonias in children simulating pulmonary and mediastinal masses. Radiology 1973;
106:179.
47. Grossman LK, Wald ER, Nair P, Papiez J. Roentgenographic follow-up of acute pneumonia in children. Pediatrics 1979;
63:30.
48. Virkki R, Juven T, Mertsola J, Ruuskanen O. Radiographic follow-up of pneumonia in children. Pediatr Pulmonol 2005;
40:223.
49. Gibson NA, Hollman AS, Paton JY. Value of radiological follow up of childhood pneumonia. BMJ 1993; 307:1117.
50. Heaton P, Arthur K. The utility of chest radiography in the follow-up of pneumonia. N Z Med J 1998; 111:315.

51. Wacogne I, Negrine RJ. Are follow up chest x ray examinations helpful in the management of children recovering from
pneumonia? Arch Dis Child 2003; 88:457.
52. Surn P, Try K, Eriksson J, et al. Radiographic follow-up of community-acquired pneumonia in children. Acta Paediatr
2008; 97:46.
53. Clark CE, Coote JM, Silver DA, Halpin DM. Asthma after childhood pneumonia: six year follow up study. BMJ 2000;
320:1514.
Topic 5987 Version 17.0

GRAPHICS Severity of community acquired pneumonia in infants and children

Clinical features of mild pneumonia

Clinical features of severe pneumonia

Temperature <38.5C (101.3F)

Temperature 38.5C (101.3F)

Mild or absent respiratory distress:

Moderate to severe respiratory distress:

Increased RR, but less than the age-specific RR that defines

moderate to severe respiratory distress

RR >70 breaths/minute for infants; RR >50 breaths/minute

for older children

Mild or absent retractions

No grunting

Moderate/severe suprasternal, intercostal, or subcostal

retractions (<12 months)

No nasal flaring

Severe difficulty breathing (12 months)

No apnea

Grunting

Mild shortness of breath

Nasal flaring

Apnea

Significant shortness of breath

Normal color

Cyanosis

Normal mental status

Altered mental status

Normoxemia (oxygen saturation 92 percent in room air)

Hypoxemia (sustained oxygen saturation <90 percent in

room air at sea level)

Normal feeding (infants); no vomiting

Not feeding (infants) or signs of dehydration (older children)

Normal heart rate

Tachycardia

Capillary refill <2 seconds

Capillary refill 2 seconds

RR: respiratory rate. Data from: Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired
pneumonia in infants and children older than 3 months of age: Clinical practice guidelines by the Pediatric Infectious Diseases
Society and the Infectious Diseases Society of America. Clin Infect Dis 2011; 53:e25. Harris M, Clark J, Coote N, et al. British
Thoracic Society guidelines for the management of community acquired pneumonia in children: update 2011. Thorax 2011;
66:ii1.

Initial oral empiric antibiotics for outpatient treatment of pediatric communityacquired pneumonia
Age group

Empiric regimen

1 to 6 months

Bacterial (not Chlamydia

trachomatis)

Infants <3 to 6 months of age with suspected bacterial pneumonia should be

hospitalized

Chlamydia trachomatis

See UpToDate topic on Chlamydia trachomatis infections in the newborn

6 months to 5 years

Typical bacterial*

Amoxicillin 90 mg/kg per day in 2 or 3 divided doses (MAX 4 g/day), OR

Amoxicillin-clavulanate 90 mg/kg per day of the amoxicillin component in 2 or 3 divided

doses (MAX 4 g/day amoxicillin component), OR

For patients with non type 1 hypersensitivity to penicillins:

- Cefdinir 14 mg/kg per day in 2 divided doses (MAX 600 mg/day), OR

For patients with type 1 hypersensitivity to penicillins:

- Clindamycin 30 to 40 mg/kg per day in 3 or 4 divided doses (MAX 1.8 g/day), OR

- Erythromycin 30 to 50 mg/kg per day in 4 divided doses (MAX 2 g/day as base, 3.2
g/day as ethylsuccinate), OR

- Azithromycin 10 mg/kg on day 1 followed by 5 mg/kg daily for 4 more days (MAX 500
mg on day 1 and 250 mg thereafter), OR

- Clarithromycin 15 mg/kg per day in 2 divided doses (MAX 1 g/day), OR

In communities with a high rate of pneumococcal resistance to penicillin:

- Linezolid 30 mg/kg per day in 3 divided doses (MAX 1800 mg/day), OR

- Levofloxacin 16 to 20 mg/kg per day in 2 divided doses (MAX 750 mg/day)

5 years

Mycoplasma pneumoniae or

Erythromycin 40 to 50 mg/kg per day in 4 divided doses (MAX 2 g/day as base, 3.2 g/day

Chlamydophila pneumoniae

as ethylsuccinate), OR

Azithromycin 10 mg/kg on day 1 followed by 5 mg/kg daily for 4 more days (MAX 500 mg on
day 1 and 250 mg thereafter), OR

Clarithromycin 15 mg/kg per day in 2 divided doses (MAX 1 g/day), OR

Doxycycline 4 mg/kg per day in 2 divided doses (MAX 200 mg/day), OR

For skeletally mature patients:

- Levofloxacin 8 to 10 mg/kg once daily for children 5 to 16 years (MAX 500 mg/day);
500 mg once per day for children for children 16 years, OR

- Moxifloxacin 400 mg once per day

Typical bacterial*

Amoxicillin 90 mg/kg per day in 2 or 3 divided doses (MAX 4 g/day), OR

For patients with non type 1 hypersensitivity to penicillins:

- Cefdinir 14 mg/kg per day in 2 divided doses (MAX 600 mg/day), OR

- Cefpodoxime 10 mg/kg per day in 2 divided doses (MAX 400 mg/day), OR

For patients with type 1 hypersensitivity to penicillins:

- Clindamycin 30 to 40 mg/kg per day in 3 or 4 divided doses (MAX 1.8 g/day), OR

- Erythromycin 40 to 50 mg/kg per day in 4 divided doses (MAX 2 g/day as base, 3.2
g/day as ethyl succinate), OR

- Azithromycin 10 mg/kg on day 1 followed by 5 mg/kg daily for 4 more days (MAX 500
mg on day 1 and 250 mg thereafter), OR

- Clarithromycin 15 mg/kg per day in 2 divided doses (MAX 1 g/day), OR

In communities with a high rate of pneumococcal resistance to penicillin:

- Linezolid 30 mg/kg per day divided in 3 doses (MAX 1800 mg/day) for children <12
years; 20 mg/kg per day divided in 2 doses (MAX 1200 mg/day) for children 12 years,
OR

- Levofloxacin 8 to 10 mg/kg once daily for children 5 to 16 years (MAX 750 mg/day); 750

mg once daily for children 16 years

Aspiration pneumonia

Community-acquired

Amoxicillin-clavulanate 40 to 50 mg/kg per day in 2 or 3 divided doses (MAX 1750 mg/day

amoxicillin component), OR

For patients with type 1 hypersensitivity to beta-lactam antibiotics:

- Clindamycin 30 to 40 mg/kg per day, divided in 3 or 4 doses (MAX 1.8 g/day)

CAP: community-acquired pneumonia; MAX: maximum. * 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. Preferred agent. Should be used with
caution in patients under the age of eight years. Also covers typical bacterial pathogens. Data from: McIntosh K.
Community-acquired pneumonia in children. N Engl J Med 2002; 346:429. Bradley JS, Byington CL, Shah SS, et al. The
management of community-acquired pneumonia in infants and children older than 3 months of age: Clinical practice
guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis 2011;
53:e25. American Academy of Pediatrics. Antibacterial drugs for pediatric patients beyond the newborn period. In: Red Book:
2009 Report of the Committee on Infectious Diseases, 28th ed. American Academy of Pediatrics, Elk Grove Village, IL 2009.
p.747.

Groups at high risk for influenza complications

Children <2 years*

Adults 65 years of age

Persons with chronic pulmonary (including asthma), cardiovascular (except hypertension), renal, hepatic, hematologic (including
sickle cell disease), metabolic (including diabetes mellitus), neurologic, neuromuscular, and neurodevelopmental disorders (including
disorders of the brain, spinal cord, peripheral nerve and muscle such as cerebral palsy, epilepsy, stroke, intellectual disability [mental
retardation], moderate to severe developmental delay, muscular dystrophy, or spinal cord injury)

Immunosuppression (including immunosuppression caused by medications or by human immunodeficiency virus)

Women who are pregnant or postpartum (within 2 weeks after delivery)

Children <19 years of age and receiving long-term aspirin therapy

Native Americans and Alaskan Natives

Morbidly obese (body mass index [BMI] 40 for adults or BMI >2.33 standard deviations above the mean for children)

Residents of nursing homes and other chronic care facilities

* Although all children <5 years of age are considered to be at higher risk for complications of influenza, the highest risk is
for those <2 years of age, with the highest hospitalization and death rates among infants <6 months of age. Adapted from:
Centers for Disease Control and Prevention. 2011-2012 Influenza antiviral medications: Summary for clinicians.
http://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm (Accessed on June 28, 2012).

Gell and Coombs classification of immunologic reactions

Type

I
Immediate
reaction
(within 1
hour)

II

Description
IgE-mediated,
immediate-type
hypersensitivity

Mechanism
Antigen exposure causes IgE-mediated
activation of mast cells and basophils, with
release of vasoactive substances such as
histamine, prostaglandins, and leukotrienes.

Clinical features

Anaphylaxis
Angioedema
Bronchospasm
Urticaria (hives)

Antibodydependent
cytotoxicity

An antigen or hapten that is intimately

associated with a cell binds to antibody,
leading to cell or tissue injury

Hemolytic anemia
Thrombocytopenia
Neutropenia

III

Immune complex
disease

Damage is caused by formation or deposition

of antigen-antibody complexes in vessels or
tissue. Deposition of immune complexes
causes complement activation and/or
recruitment of neutrophils by interaction of
immune complexes with Fc IgG receptors

Serum sickness

IV

Cell-mediated or
delayed
hypersensitivity

Antigen exposure activates T cells, which then

mediate tissue injury. Depending upon the type
of T cell activation and the other effector cells
recruited, different subtypes can be
differentiated (ie, Types IVa-IVd)

Contact dermatitis, some morbilliform

reactions, severe exfoliative dermatoses
(eg, SJS/TEN), AGEP, DRESS/DiHS,
interstitial nephritis, drug-induced
hepatitis, other presentations

SJS/TEN: Stevens-Johnson syndrome/ Toxic epidermal necrolysis AGEP: Acute generalized exanthematous
pustulosis DRESS/DiHS: Drug rash with eosinophilia and systemic symptoms/Drug-induced
hypersensitivity syndrome Adapted from: Weiss ME, Adkinson NF. Immediate hypersensitivity reactions to penicillin and
related antibiotics. Clin Allergy 1988; 18:515.
2013 UpToDate, Inc. All rights reserved. |Subscription and License Agreement|Release: 21.1 - C21.12
Licensed to: Inst Chihuahuense de Salud|Support Tag: [1103-189.254.162.24-A17C8A0CD7-494946.14]

Official reprint from UpToDate www.uptodate.com

2013 UpToDate
Print|Back

Inpatient treatment of pneumonia in children

Author
William J Barson, MD
Section Editors
Morven S Edwards, MD
George B Mallory, MD
Deputy Editor
Mary M Torchia, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2013. |This topic last updated: ene 8, 2013.
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 communityacquired 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 [SpO2] <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 [SpO2] >92
percent in FiO2 >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)

PaO2/FiO2 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 [SpO2] <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 "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 (SpO2) 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 thirdgeneration 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 thirdgeneration 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 macrolideresistant 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 lifethreatening 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, increasing clindamycin 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 gramnegative 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 gramnegative 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 broadspectrum 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 possibly trimethoprim-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 communityacquired 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 20 mm/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 (SpO2)

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 communityacquired 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 childs 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 communityacquired 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
th

th

the Basics. The Basics patient education pieces are written in plain language, at the 5 to 6 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
th

th

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 to 12 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. Followup 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.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES

1. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and children
older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious
Diseases Society of America. Clin Infect Dis 2011; 53:e25.
2. Harris M, Clark J, Coote N, et al. British Thoracic Society guidelines for the management of community acquired
pneumonia in children: update 2011. Thorax 2011; 66 Suppl 2:ii1.
3. Russell G. Community acquired pneumonia. Arch Dis Child 2001; 85:445.
4. McIntosh K. Community-acquired pneumonia in children. N Engl J Med 2002; 346:429.
5. Duncan H, Hutchison J, Parshuram CS. The Pediatric Early Warning System score: a severity of illness score to predict
urgent medical need in hospitalized children. J Crit Care 2006; 21:271.
6. Siegel JD, Rhinehart E, Jackson M, et al. 2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious
Agents in Healthcare Settings. http://www.cdc.gov/hicpac/2007ip/2007isolationprecautions.html (Accessed on September
25, 2011).
7. Khoshoo V, Edell D. Previously healthy infants may have increased risk of aspiration during respiratory syncytial viral
bronchiolitis. Pediatrics 1999; 104:1389.
8. Singhi S, Dhawan A. Frequency and significance of electrolyte abnormalities in pneumonia. Indian Pediatr 1992; 29:735.
9. Dhawan A, Narang A, Singhi S. Hyponatraemia and the inappropriate ADH syndrome in pneumonia. Ann Trop Paediatr
1992; 12:455.
10. Britton S, Bejstedt M, Vedin L. Chest physiotherapy in primary pneumonia. Br Med J (Clin Res Ed) 1985; 290:1703.
11. Levine A. Chest physical therapy for children with pneumonia. J Am Osteopath Assoc 1978; 78:122.
12. Stapleton T. Chest physiotherapy in primary pneumonia. Br Med J (Clin Res Ed) 1985; 291:143.
13. Paludo C, Zhang L, Lincho CS, et al. Chest physical therapy for children hospitalised with acute pneumonia: a
randomised controlled trial. Thorax 2008; 63:791.
14. Lukrafka JL, Fuchs SC, Fischer GB, et al. Chest physiotherapy in paediatric patients hospitalised with communityacquired pneumonia: a randomised clinical trial. Arch Dis Child 2012; 97:967.
15. Low DE, Pichichero ME, Schaad UB. Optimizing antibacterial therapy for community-acquired respiratory tract infections
in children in an era of bacterial resistance. Clin Pediatr (Phila) 2004; 43:135.
16. Friis B, Andersen P, Brene E, et al. Antibiotic treatment of pneumonia and bronchiolitis. A prospective randomised study.
Arch Dis Child 1984; 59:1038.
17. Esposito S, Bosis S, Cavagna R, et al. Characteristics of Streptococcus pneumoniae and atypical bacterial infections in
children 2-5 years of age with community-acquired pneumonia. Clin Infect Dis 2002; 35:1345.
18. Virkki R, Juven T, Rikalainen H, et al. Differentiation of bacterial and viral pneumonia in children. Thorax 2002; 57:438.

19. Mani CS, Murray DL. Acute pneumonia and its complications. In: Principles and Practice of Pediatric Infectious Diseases,
4th, Long SS, Pickering LK, Prober CG. (Eds), Elsevier Saunders, Edinburgh 2012. p.235.
20. Pelton SI, Hammerschlag MR. Overcoming current obstacles in the management of bacterial community-acquired
pneumonia in ambulatory children. Clin Pediatr (Phila) 2005; 44:1.
21. Juvn T, Mertsola J, Waris M, et al. Etiology of community-acquired pneumonia in 254 hospitalized children. Pediatr Infect
Dis J 2000; 19:293.
22. Korppi M, Heiskanen-Kosma T, Jalonen E, et al. Aetiology of community-acquired pneumonia in children treated in
hospital. Eur J Pediatr 1993; 152:24.
23. Heiskanen-Kosma T, Korppi M, Jokinen C, et al. Etiology of childhood pneumonia: serologic results of a prospective,
population-based study. Pediatr Infect Dis J 1998; 17:986.
24. Trujillo M, McCracken GH Jr. Prolonged morbidity in children with group A beta-hemolytic streptococcal pneumonia.
Pediatr Infect Dis J 1994; 13:411.
25. Drummond P, Clark J, Wheeler J, et al. Community acquired pneumonia--a prospective UK study. Arch Dis Child 2000;
83:408.
26. Bradley JS. Management of community-acquired pediatric pneumonia in an era of increasing antibiotic resistance and
conjugate vaccines. Pediatr Infect Dis J 2002; 21:592.
27. American Academy of Pediatrics. Antimicrobial agents and related therapy. In: Red Book: 2012 Report of the Committee
on Infectious Diseases, 29th, Pickering LK. (Ed), American Academy of Pediatrics, Elk Grove Village, IL 2012. p.799.
28. Buckingham SC, Brown SP, Joaquin VH. Breakthrough bacteremia and meningitis during treatment with cephalosporins
parenterally for pneumococcal pneumonia. J Pediatr 1998; 132:174.
29. Dowell SF, Smith T, Leversedge K, Snitzer J. Failure of treatment of pneumonia associated with highly resistant
pneumococci in a child. Clin Infect Dis 1999; 29:462.
30. Atkinson M, Lakhanpaul M, Smyth A, et al. Comparison of oral amoxicillin and intravenous benzyl penicillin for community
acquired pneumonia in children (PIVOT trial): a multicentre pragmatic randomised controlled equivalence trial. Thorax
2007; 62:1102.
31. Flood RG, Badik J, Aronoff SC. The utility of serum C-reactive protein in differentiating bacterial from nonbacterial
pneumonia in children: a meta-analysis of 1230 children. Pediatr Infect Dis J 2008; 27:95.
32. Yamada M, Buller R, Bledsoe S, Storch GA. Rising rates of macrolide-resistant Mycoplasma pneumoniae in the central
United States. Pediatr Infect Dis J 2012; 31:409.
33. Davidson R, Cavalcanti R, Brunton JL, et al. Resistance to levofloxacin and failure of treatment of pneumococcal
pneumonia. N Engl J Med 2002; 346:747.
34. Kaplan SL, Mason EO Jr, Barson WJ, et al. Outcome of invasive infections outside the central nervous system caused by
Streptococcus pneumoniae isolates nonsusceptible to ceftriazone in children treated with beta-lactam antibiotics. Pediatr
Infect Dis J 2001; 20:392.
35. Bradley JS. Old and new antibiotics for pediatric pneumonia. Semin Respir Infect 2002; 17:57.
36. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the
treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52:e18.
37. Rybak M, Lomaestro B, Rotschafer JC, et al. Therapeutic monitoring of vancomycin in adult patients: a consensus review
of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society of
Infectious Diseases Pharmacists. Am J Health Syst Pharm 2009; 66:82.
38. McKamy S, Hernandez E, Jahng M, et al. Incidence and risk factors influencing the development of vancomycin
nephrotoxicity in children. J Pediatr 2011; 158:422.
39. Sandora TJ, Harper MB. Pneumonia in hospitalized children. Pediatr Clin North Am 2005; 52:1059.
40. Hoffer FA, Bloom DA, Colin AA, Fishman SJ. Lung abscess versus necrotizing pneumonia: implications for interventional
therapy. Pediatr Radiol 1999; 29:87.
41. Kerem E, Bar Ziv Y, Rudenski B, et al. Bacteremic necrotizing pneumococcal pneumonia in children. Am J Respir Crit
Care Med 1994; 149:242.
42. McCarthy VP, Patamasucon P, Gaines T, Lucas MA. Necrotizing pneumococcal pneumonia in childhood. Pediatr
Pulmonol 1999; 28:217.
43. Tan TQ, Seilheimer DK, Kaplan SL. Pediatric lung abscess: clinical management and outcome. Pediatr Infect Dis J 1995;
14:51.
44. Rice TW, Ginsberg RJ, Todd TR. Tube drainage of lung abscesses. Ann Thorac Surg 1987; 44:356.
45. Zuhdi MK, Spear RM, Worthen HM, Peterson BM. Percutaneous catheter drainage of tension pneumatocele, secondarily
infected pneumatocele, and lung abscess in children. Crit Care Med 1996; 24:330.
46. Emanuel B, Shulman ST. Lung abscess in infants and children. Clin Pediatr (Phila) 1995; 34:2.
47. Kunyoshi V, Cataneo DC, Cataneo AJ. Complicated pneumonias with empyema and/or pneumatocele in children. Pediatr
Surg Int 2006; 22:186.
48. Ceruti E, Contreras J, Neira M. Staphylococcal pneumonia in childhood. Long-term follow-up including pulmonary function
studies. Am J Dis Child 1971; 122:386.
49. Soto M, Demis T, Landau LI. Pulmonary function following staphylococcal pneumonia in children. Aust Paediatr J 1983;
19:172.

50. Amitai I, Mogle P, Godfrey S, Aviad I. Pneumatocele in infants and children. Report of 12 cases. Clin Pediatr (Phila) 1983;
22:420.
51. Dagan R, Syrogiannopoulos G, Ashkenazi S, et al. Parenteral-oral switch in the management of paediatric pneumonia.
Drugs 1994; 47 Suppl 3:43.
52. Dunbar LM, Wunderink RG, Habib MP, et al. High-dose, short-course levofloxacin for community-acquired pneumonia: a
new treatment paradigm. Clin Infect Dis 2003; 37:752.
53. Mandell LA, File TM Jr. Short-course treatment of community-acquired pneumonia. Clin Infect Dis 2003; 37:761.
54. Alves dos Santos JW, Torres A, Michel GT, et al. Non-infectious and unusual infectious mimics of community-acquired
pneumonia. Respir Med 2004; 98:488.
55. Hyde TB, Gay K, Stephens DS, et al. Macrolide resistance among invasive Streptococcus pneumoniae isolates. JAMA
2001; 286:1857.
56. Lahti E, Peltola V, Waris M, et al. Induced sputum in the diagnosis of childhood community-acquired pneumonia. Thorax
2009; 64:252.
57. Morales JO, Snead H. Efficacy and safety of intravenous cefotaxime for treating pneumonia in outpatients. Am J Med
1994; 97:28.
58. Esposito S. Treatment of lower respiratory tract infections in Italy: the role of outpatient parenteral antibiotic therapy.
Chemotherapy 2001; 47 Suppl 1:33.
59. Tice AD, Rehm SJ, Dalovisio JR, et al. Practice guidelines for outpatient parenteral antimicrobial therapy. IDSA
guidelines. Clin Infect Dis 2004; 38:1651.
60. Gaston B. Pneumonia. Pediatr Rev 2002; 23:132.
61. Jadavji T, Law B, Lebel MH, et al. A practical guide for the diagnosis and treatment of pediatric pneumonia. CMAJ 1997;
156:S703.
62. Griscom NT. Pneumonia in children and some of its variants. Radiology 1988; 167:297.
63. McLennan MK. Radiology rounds. Round pneumonia. Can Fam Physician 1998; 44:751, 757.
64. Kim YW, Donnelly LF. Round pneumonia: imaging findings in a large series of children. Pediatr Radiol 2007; 37:1235.
65. Eggli KD, Newman B. Nodules, masses, and pseudomasses in the pediatric lung. Radiol Clin North Am 1993; 31:651.
66. Rose RW, Ward BH. Spherical pneumonias in children simulating pulmonary and mediastinal masses. Radiology 1973;
106:179.
67. Donnelly LF. Maximizing the usefulness of imaging in children with community-acquired pneumonia. AJR Am J
Roentgenol 1999; 172:505.
68. Grossman LK, Wald ER, Nair P, Papiez J. Roentgenographic follow-up of acute pneumonia in children. Pediatrics 1979;
63:30.
69. Virkki R, Juven T, Mertsola J, Ruuskanen O. Radiographic follow-up of pneumonia in children. Pediatr Pulmonol 2005;
40:223.
70. Gibson NA, Hollman AS, Paton JY. Value of radiological follow up of childhood pneumonia. BMJ 1993; 307:1117.
71. Heaton P, Arthur K. The utility of chest radiography in the follow-up of pneumonia. N Z Med J 1998; 111:315.
72. Wacogne I, Negrine RJ. Are follow up chest x ray examinations helpful in the management of children recovering from
pneumonia? Arch Dis Child 2003; 88:457.
73. Surn P, Try K, Eriksson J, et al. Radiographic follow-up of community-acquired pneumonia in children. Acta Paediatr
2008; 97:46.
74. Bruckheimer E, Dolberg S, Shlesinger Y, et al. Primary lung abscess in infancy. Pediatr Pulmonol 1995; 19:188.
75. Clark CE, Coote JM, Silver DA, Halpin DM. Asthma after childhood pneumonia: six year follow up study. BMJ 2000;
320:1514.
76. Eastham KM, Hammal DM, Parker L, Spencer DA. A follow-up study of children hospitalised with community-acquired
pneumonia. Arch Dis Child 2008; 93:755.
77. Jokinen C, Heiskanen L, Juvonen H, et al. Incidence of community-acquired pneumonia in the population of four
municipalities in eastern Finland. Am J Epidemiol 1993; 137:977.
78. Feikin DR, Schuchat A, Kolczak M, et al. Mortality from invasive pneumococcal pneumonia in the era of antibiotic
resistance, 1995-1997. Am J Public Health 2000; 90:223.
Topic 6054 Version 21.0

GRAPHICS Severity of community acquired pneumonia in infants and children

Clinical features of mild pneumonia

Clinical features of severe pneumonia

Temperature <38.5C (101.3F)

Temperature 38.5C (101.3F)

Mild or absent respiratory distress:

Moderate to severe respiratory distress:

Increased RR, but less than the age-specific RR that defines

moderate to severe respiratory distress

RR >70 breaths/minute for infants; RR >50 breaths/minute

for older children

Mild or absent retractions

No grunting

Moderate/severe suprasternal, intercostal, or subcostal

retractions (<12 months)

No nasal flaring

Severe difficulty breathing (12 months)

No apnea

Grunting

Mild shortness of breath

Nasal flaring

Apnea

Significant shortness of breath

Normal color

Cyanosis

Normal mental status

Altered mental status

Normoxemia (oxygen saturation 92 percent in room air)

Hypoxemia (sustained oxygen saturation <90 percent in

room air at sea level)

Normal feeding (infants); no vomiting

Not feeding (infants) or signs of dehydration (older children)

Normal heart rate

Tachycardia

Capillary refill <2 seconds

Capillary refill 2 seconds

RR: respiratory rate. Data from: Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired
pneumonia in infants and children older than 3 months of age: Clinical practice guidelines by the Pediatric Infectious Diseases
Society and the Infectious Diseases Society of America. Clin Infect Dis 2011; 53:e25. Harris M, Clark J, Coote N, et al. British
Thoracic Society guidelines for the management of community acquired pneumonia in children: update 2011. Thorax 2011;
66:ii1.

Parenteral empiric antibiotics for inpatient treatment of pediatric pneumonia

Age group and suspected pathogens
1 to 6 months

Suggested empiric regimens*

Bacterial (not Chlamydia trachomatis or

Staphylococcus aureus)

Ceftriaxone 50 to 100 mg/kg per day in 1 or 2 divided doses (2 doses should

be used for severe infection or substantial local penicillin resistance), OR
Cefotaxime 150 mg/kg per day in 3 or 4 divided doses (4 doses should be
used for severe infection or substantial local penicillin resistance)

Chlamydia trachomatis

>6 months

Uncomplicated bacterial (not Mycoplasma

pneumoniae, Chlamydophila pneumoniae, or
S. aureus)

Ampicillin 150 to 200 mg/kg per day in 4 divided doses (MAX 12 g/day), OR

Penicillin G 200,000 to 250,000 units/kg per day in 4 or 6 divided doses, OR

Cefotaxime 150 mg/kg per day in 3 divided doses (MAX 8 g/day or 10 g/day
divided in 4 doses for severe infection or substantial local penicillin
resistance), OR

Ceftriaxone 50 to 100 mg/kg per day in 1 or 2 divided doses (MAX 2 g/day or

4 g/day divided in 2 doses for severe infection or substantial local penicillin
resistance)

M. pneumoniae or C. pneumoniae

Azithromycin 10 mg/kg once per day for two days (MAX 500 mg/day);
transition to oral therapy at 5 mg/kg per day as soon as clinically appropriate,
OR

Erythromycin 20 mg/kg per day in 4 divided doses (MAX 4 g/day), OR

Levofloxacin 16 to 20 mg/kg per day in 2 divided doses for children 6 months
to 5 years; 8 to 10 mg/kg per day for children 5 to 16 years (MAX 750 mg)

Suggested empiric regimens

Syndrome

Severe pneumonia (see text for clinical features)

Ceftriaxone 100 mg/kg per day in 2 divided doses (MAX 4 g/day), OR

Cefotaxime 150 mg/kg per day in 4 divided doses (MAX 10 g/day)
PLUS
Azithromycin 10 mg/kg once per day for two days (MAX 500 mg/day);
transition to oral therapy at 5 mg/kg per day as soon as clinically appropriate,
OR

Erythromycin 20 mg/kg per day in 4 divided doses (MAX 4 g/day), OR

Doxycycline** 4 mg/kg per day in 2 divided doses (MAX 200 mg/day);
transition to oral therapy as soon as clinically appropriate

Severe pneumonia requiring ICU admission (see

text for details)

Vancomycin 60 mg/kg per day in 4 divided doses (MAX 4 g/day) PLUS either
Ceftriaxone 100 mg/kg per day in 2 divided doses (MAX 4 g/day) or
Cefotaxime 150 mg/kg per day in 4 divided doses (MAX 10 g/day)
PLUS
Azithromycin 10 mg/kg once per day for two days (MAX 500 mg/day);
transition to oral therapy at 5 mg/kg per day as soon as clinically appropriate
PLUS (if necessary)
Nafcillin

150 mg/kg per day in 4 or 6 divided doses (MAX 12 g/day)

PLUS (if indicated)

Antiviral treatment for influenza

Complicated pneumonia/abscess

Ceftriaxone 100 mg/kg per day in 2 divided doses (MAX 4 g/day) or

Cefotaxime 150 mg/kg per day in 4 divided doses (MAX 10 g/day)
PLUS (if necessary)

Clindamycin 30 to 40 mg/kg per day in 3 or 4 divided doses (MAX 3.6 g/day)

or, for patients allergic to clindamycin,
Vancomycin 40 to 60 mg/kg per day in 3 or 4 divided doses (MAX 4 g/day)

Nosocomial (hospital-acquired) pneumonia

Gentamicin 7.5 mg/kg per day divided in 3 doses for children <5 years; 6 to
7.5 mg/kg per day divided in 3 doses for children 5 years or Amikacin 15 to
22.5 mg/kg per day divided in 3 doses, PLUS
Piperacillin-tazobactam 300 mg/kg per day in 4 divided doses (MAX 16 g/day),
OR
Ticarcillin-clavulanate 300 mg/kg per day in 4 or 6 divided doses (MAX 24
g/day), OR
Meropenem 60 mg/kg per day in 3 divided doses (MAX 3 g/day), OR
Ceftazidime 125 to 150 mg/kg per day in 3 divided doses (MAX 6 g/day), OR
Cefepime 150 mg/kg per day in 3 divided doses (MAX 4 g/day), OR
Clindamycin 30 to 40 mg/kg per day in 3 or 4 divided doses (MAX 3.6 g/day)

Community-acquired aspiration pneumonia

Ampicillin-sulbactam 150 to 200 mg/kg per day in 4 divided doses (MAX 8

g/day of ampicillin component)
OR, if MRSA is a consideration,
Clindamycin 30 to 40 mg/kg per day in 3 or 4 divided doses (MAX 3.6 g/day)

Hospital-acquired aspiration pneumonia in

patients colonized with unusual gram-negative
,
pathogens ***

Piperacillin-tazobactam 300 mg/kg per day in 4 divided doses (MAX 16 g/day),

OR
Ticarcillin-clavulanate 300 mg/kg per day in 4 or 6 divided doses (MAX 24
g/day), OR
Meropenem 60 mg/kg per day in 3 divided doses (MAX 3 g/day)

MAX: maximum dose; ICU: intensive care unit; MRSA: methicillin-resistant Staphylococcus aureus. * Consultation with a
specialist in infectious diseases for children is suggested for children with severe hypersensitivity to beta-lactam antibiotics
(eg, penicillins and cephalosporins). Add vancomycin 40 to 60 mg/kg per day in 3 or 4 divided doses or clindamycin 30 to
40 mg/kg per day in 3 or 4 divided doses for suspected community-associated methicillin resistant S. aureus pneumonia.
The 100 mg/kg per day dose of ceftriaxone should be used only if local rates of penicillin resistance to Streptococcus
pneumoniae are substantial. Fully immunized with conjugate vaccines for Haemophilus influenzae type b (Hib) and S.
pneumoniae in communities where penicillin resistance in invasive strains of pneumococcus is insignificant. Not fully
immunized with conjugate vaccines for Hib and S. pneumoniae or in communities where penicillin resistance in invasive
strains of pneumococcus is significant. Parenteral erythromycin is associated with phlebitis, prokinetic and, rarely,
cardiotoxic effects. Dosages recommended are for patients with normal renal function. Children of any age with severe
infection may benefit from broad-spectrum therapy that addresses both atypical and typical pathogens. ** Should be used
with caution under the age of 8 years. These recommendations are for children of any age. If S. aureus is likely, since
methicillin-sensitive S. aureus is more rapidly killed by nafcillin than by vancomycin. Pneumonia complicated by
significant parapneumonic effusion or necrotizing process (S. pneumoniae, S. aureus, and Streptococcus pyogenes are
possible pathogens). If MRSA is a consideration. The aminoglycoside/meropenem combination should be used if
extended-spectrum or Amp C beta-lactamase-producing gram-negative rods are possible etiologies. The
aminoglycoside/cephalosporin combination should not be used if aspiration pneumonia is a possibility. Vancomycin should be
added to the empiric regimen if MRSA is a consideration. Gentamicin dosage is adjusted for peak concentration of 7 to 9
mcg/mL and trough of <2 mcg/mL. Patients with severe hypersensitivity reaction to beta-lactam antibiotics can be
treated with a combination of clindamycin plus an aminoglycoside. *** Vancomycin should be added to the empiric regimen
if MRSA is a consideration. Data from: McIntosh K. Community-acquired pneumonia in children. N Engl J Med 2002;
346:429. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and
children older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the
Infectious Diseases Society of America. Clin Infect Dis 2011; 53:e25. American Academy of Pediatrics. Antimicrobial agents
and related therapy. In: Red Book: 2012 Report of the Committee on Infectious Diseases, 29th, Pickering LK. (Ed), American
Academy of Pediatrics, Elk Grove Village, IL 2012. p.799.

Clinical and radiographic clues to the etiology of pneumonia in children*

Etiology

Bacteria(most commonly Streptococcus

pneumoniae)

Atypical bacterial(Mycoplasma
pneumoniae, Chlamydophila
pneumoniae)

Radiographic
features

Clinical features

Children of all ages

Alveolar infiltrates

Abrupt onset

Segmental consolidation

Ill-appearance

Lobar consolidation

Chills

"Round" pneumonia

Moderate to severe respiratory distress

Focal auscultatory findings

Localized chest pain

WBC count >15,000/microL (if obtained)

Elevated acute phase reactants (if obtained)

Complications:

Pleural
effusion/empyema

Lung abscess

Necrotizing pneumonia

Pneumatocele
Interstitial infiltrates

Children of all ages (most common in children >5 years)

Abrupt onset with constitutional findings (malaise, myalgia,

headache, conjunctivitis, photophobia, sore throat,
headache)

Gradually worsening nonproductive cough

Wheezing

Extrapulmonary manifestations or complications (eg,

Stevens-Johnson syndrome, hemolytic anemia, hepatitis,
etc)

Usually children <5 years

Gradual onset

Preceding upper airway symptoms

Non-toxic appearing

Diffuse, bilateral auscultatory findings

Wheezing

May have associated rash (eg, measles, varicella)

Usually in infants 2 weeks to 4 months

Insidious onset

Rhinorrhea

Staccato cough pattern

Peripheral eosinophilia (if CBC obtained)

Fungal

Appropriate geographic or environmental exposure

Mediastinal or hilar
adenopathy

Mycobacterium tuberculosis

Children of any age

Mediastinal or hilar
adenopathy

Chronic cough

Constitutional symptoms

Exposure history

Viral

Afebrile pneumonia of infancy (most

commonly Chlamydia trachomatis)

Interstitial infiltrates

Hyperinflation with
interstitial process

WBC: white blood cell; CBC: complete blood count. * The clinical features frequently overlap and cannot reliably distinguish
between bacterial, atypical bacterial, and viral etiologies; up to one-half of community-acquired pneumonias in children may
be mixed bacterial/viral infections. Chest radiography generally is not helpful in determining the potential causative agent of
pneumonia. Nonetheless, these features may facilitate decisions regarding empiric therapy. Data from: Bartlett JG, Mundy
LM. Community-acquired pneumonia. N Engl J Med 1995; 333:1618. Boyer KM. Nonbacterial pneumonia. In: Textbook of
Pediatric Infectious Diseases, 6th ed, Feigin RD, Cherry JD, Demmler-Harrison GJ, Kaplan SL (Eds), Saunders, Philadelphia
2009. p.289. Broughton RA. Infections due to Mycoplasma pneumoniae in childhood. Pediatr Infect Dis 1986; 5:71. McIntosh
K. Community-acquired pneumonia in children. N Engl J Med 2002; 346:429.

Gell and Coombs classification of immunologic reactions

Type

I
Immediate
reaction
(within 1
hour)

II

Description
IgE-mediated,
immediate-type
hypersensitivity

Mechanism
Antigen exposure causes IgE-mediated
activation of mast cells and basophils, with
release of vasoactive substances such as
histamine, prostaglandins, and leukotrienes.

Clinical features

Anaphylaxis
Angioedema
Bronchospasm
Urticaria (hives)

Antibodydependent
cytotoxicity

An antigen or hapten that is intimately

associated with a cell binds to antibody,
leading to cell or tissue injury

Hemolytic anemia
Thrombocytopenia
Neutropenia

III

Immune complex
disease

Damage is caused by formation or deposition

of antigen-antibody complexes in vessels or
tissue. Deposition of immune complexes
causes complement activation and/or
recruitment of neutrophils by interaction of
immune complexes with Fc IgG receptors

Serum sickness

IV

Cell-mediated or
delayed
hypersensitivity

Antigen exposure activates T cells, which then

mediate tissue injury. Depending upon the type
of T cell activation and the other effector cells
recruited, different subtypes can be
differentiated (ie, Types IVa-IVd)

Contact dermatitis, some morbilliform

reactions, severe exfoliative dermatoses
(eg, SJS/TEN), AGEP, DRESS/DiHS,
interstitial nephritis, drug-induced
hepatitis, other presentations

SJS/TEN: Stevens-Johnson syndrome/ Toxic epidermal necrolysis AGEP: Acute generalized exanthematous
pustulosis DRESS/DiHS: Drug rash with eosinophilia and systemic symptoms/Drug-induced
hypersensitivity syndrome Adapted from: Weiss ME, Adkinson NF. Immediate hypersensitivity reactions to penicillin and
related antibiotics. Clin Allergy 1988; 18:515.

Specific antibiotic therapy for pneumonia in children

Pathogen

Parenteral therapy

Streptococcus
pneumoniae with MICs
for penicillin 2.0
mcg/mL

Preferred: ampicillin (150-200 mg/kg/day every

6 hours) or penicillin (200,000-250,000
units/kg/day every 4-6 hours)
Alternatives: ceftriaxone (50-100 mg/kg/day
every 12-24 hours) (preferred for parenteral
outpatient therapy) or cefotaxime (150
mg/kg/day every 8 hours); may also be effective:
clindamycin (40 mg/kg/day every 6-8 hours) or
vancomycin (40-60 mg/kg/day every 6-8 hours)

S. pneumoniae
resistant to penicillin,
with MICs 4.0 mcg/mL

Preferred: ceftriaxone (100 mg/kg/day every 1224 hours)

Alternatives: ampicillin (300-400 mg/kg/day
every 6 hours), levofloxacin (16-20 mg/kg/day
every 12 hours for children 6 months to 5 years
old and 8-10 mg/kg/day once daily for children 5
to 16 years old; maximum daily dose, 750 mg),
or linezolid (30 mg/kg/day every 8 hours for
children <12 years old and 20 mg/kg/day every
12 hours for children 12 years old); may also
be effective: clindamycin* (40 mg/kg/day every
6-8 hours) or vancomycin (40-60 mg/kg/day
every 6-8 hours)

Group A Streptococcus

Stapyhylococcus
aureus, methicillin
susceptible
(combination therapy
not well studied)

Oral therapy(step-down therapy or mild

infection)

Preferred: amoxicillin (90 mg/kg/day in 2 doses or

45 mg/kg/day in 3 doses)
Alternatives: second- or third-generation
cephalosporin (cefpodoxime, cefuroxime, cefprozil);
oral levofloxacin, if susceptible (16-20 mg/kg/day in
2 doses for children 6 months to 5 years old and 810 mg/kg/day once daily for children 5 to 16 years
old; maximum daily dose, 750 mg) or oral linezolid
(30 mg/kg/day in 3 doses for children <12 years old
and 20 mg/kg/day in 2 doses for children 12 years
old)

Preferred: oral levofloxacin (16-20 mg/kg/day in 2

doses for children 6 months to 5 years and 8-10
mg/kg/day once daily for children 5 to 16 years,
maximum daily dose, 750 mg), if susceptible, or oral
linezolid (30 mg/kg/day in 3 doses for children <12
years and 20 mg/kg/day in 2 doses for children 12
years)
Alternative: oral clindamycin* (30-40 mg/kg/day in
3 doses)

Preferred: intravenous penicillin (100,000250,000 units/kg/day every 4-6 hours) or

ampicillin (200 mg/kg/day every 6 hours)

Preferred: amoxicillin (50-75 mg/kg/day in 2

doses), or penicillin V (50-75 mg/kg/day in 3 or 4
doses)

Alternatives: ceftriaxone (50-100 mg/kg/day

every 12-24 hours) or cefotaxime (150
mg/kg/day every 8 hours); may also be effective:
clindamycin, if susceptible (40 mg/kg/day every

6-8 hours) or vancomycin (40-60 mg/kg/day

every 6-8 hours)

Alternative: oral clindamycin* (40 mg/kg/day in 3

doses)

Preferred: cefazolin (150 mg/kg/day every 8

hours) or semisynthetic penicillin, eg oxacillin
(150-200 mg/kg/day every 6-8 hours)

Preferred: oral cephalexin (75-100 mg/kg/day in 3

or 4 doses)

Alternatives: clindamycin* (40 mg/kg/day every

6-8 hours) or vancomycin (40-60 mg/kg/day
every 6-8 hours)

Alternative: oral clindamycin* (30-40 mg/kg/day in

3 or 4 doses)

S. aureus, methicillin
resistant, susceptible to
clindamycin
(combination therapy
not well studied)

Preferred: vancomycin (40-60 mg/kg/day every

6-8 hours or dosing to achieve an AUC/MIC ratio
of >400) or clindamycin (40 mg/kg/day every 6-8
hours)
Alternatives: linezolid (30 mg/kg/day every 8
hours for children <12 years old and 20
mg/kg/day every 12 hours for children 12 years
old)

S. aureus, methicillin
resistant, resistant to
clindamycin
(combination therapy
not well studied)

Haemophilus influenza,
typeable (A-F) or
nontypeable

Mycoplasma
pneumoniae

Alternatives: oral linezolid (30 mg/kg/day in 3

doses for children <12 years and 20 mg/kg/day in 2
doses for children 12 years)

Preferred: vancomycin (40-60 mg/kg/day every

6-8 hours or dosing to achieve an AUC/MIC ratio
of >400)

Preferred: oral linezolid (30 mg/kg/day in 3 doses

for children <12 years and 20 mg/kg/day in 2 doses
for children 12 years old)

Alternatives: linezolid (30 mg/kg/day every 8

hours for children <12 years old and 20
mg/kg/day every 12 hours for children 12 years
old)

Alternatives: none; entire treatment course with

parenteral therapy may be required

Preferred: intravenous ampicillin (150-200

mg/kg/day every 6 hours) if -lactamase
negative, ceftriaxone (50-100 mg/kg/day every
12-24 hours) if -lactamase producing, or
cefotaxime (150 mg/kg/day every 8 hours)

Preferred: amoxicillin (75-100 mg/kg/day in 3

doses) if -lactamase negative) or amoxicillin
clavulanate (amoxicillin component, 45 mg/kg/day
in 3 doses or 90 mg/kg/day in 2 doses) if lactamase producing

Alternatives: intravenous ciprofloxacin (30

mg/kg/day every 12 hours) or intravenous
levofloxacin (16-20 mg/kg/day every 12 hours
for children 6 months to 5 years old and 8-10
mg/kg/day once daily for children 5 to 16 years
old; maximum daily dose, 750 mg)

Alternatives: cefdinir, cefixime, cefpodoxime, or

ceftibuten

Preferred: intravenous azithromycin (10 mg/kg

on days 1 and 2 of therapy; transition to oral
therapy if possible)

Preferred: azithromycin (10 mg/kg on day 1,

followed by 5 mg/kg/day once daily on days 2-5)

Alternatives: intravenous erythromycin

lactobionate (20 mg/kg/day every 6 hours) or
levofloxacin (16-20 mg/kg/day every 12 hours;
maximum daily dose, 750 mg)

Chlamydia trachomatis
or Chlamydophila
pneumoniae

Preferred: oral clindamycin (30-40 mg/kg/day in 3

or 4 doses)

Preferred: intravenous azithromycin (10 mg/kg

on days 1 and 2 of therapy; transition to oral
therapy if possible)
Alternatives: intravenous erythromycin
lactobionate (20 mg/kg/day every 6 hours) or
levofloxacin (16-20 mg/kg/day in 2 doses for
children 6 months to 5 years old and 8-10
mg/kg/day once daily for children 5 to 16 years
old; maximum daily dose, 750 mg)

Alternatives: clarithromycin (15 mg/kg/day in 2

doses) or oral erythromycin (40 mg/kg/day in 4
doses); for children >7 years old, doxycycline (2-4
mg/kg/day in 2 doses; for adolescents with skeletal
maturity, levofloxacin (500 mg once daily) or
moxifloxacin (400 mg once daily)

Preferred: azithromycin (10 mg/kg on day 1,

followed by 5 mg/kg/day once daily days 2-5)
Alternatives: clarithromycin (15 mg/kg/day in 2
doses) or oral erythromycin (40 mg/kg/day in 4
doses); for children >7 years old, doxycycline (2-4
mg/kg/day in 2 doses); for adolescents with skeletal
maturity, levofloxacin (500 mg once daily) or
moxifloxacin (400 mg once daily)

Doses for oral therapy should not exceed adult doses. AUC: area under the time versus serum concentration curve;
MIC: minimum inhibitory concentration. * Clindamycin resistance appears to be increasing in certain geographic areas
among S. pneumoniae and S. aureus infections. For -lactam-allergic children. From: Bradley JS, Byington CL, Shah SS, et
al. The management of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice
guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis 2011;
53:e25, with permission of the Infectious Diseases Society of America. Copyright 2011 Oxford University Press.

Important aspects of the history in a child with pneumonia

Historical feature
Age of the child

Possible significance

Viral etiologies are most common in infants and preschool children

Atypical bacterial pathogens are more common in school-age children

Recent viral upper respiratory tract

infection

May predispose to bacterial superinfection with Streptococcus pneumoniae or

Staphylococcus aureus

Associated symptoms

Mycoplasma pneumoniae is often associated with extrapulmonary manifestations (eg,

headache, photophobia, rash)

Presence of cough, chest pain,

shortness of breath, difficulty
breathing

"Classic" features of pneumonia, but non-specific

Increased work of breathing in the

absence of stridor or wheezing

Suggestive of severe pneumonia

Choking episode

May indicate foreign body aspiration

Duration of symptoms

Chronic cough (>4 weeks) suggests etiology other than acute pneumonia (refer to UpToDate
topic on causes of chronic cough in children)

Previous episodes

Recurrent episodes may indicate aspiration, congenital or acquired anatomic abnormality,

cystic fibrosis, immunodeficiency, asthma, missed foreign body

Immunization status

Completion of the primary series of immunizations for Haemophilus influenzae type b,

Streptococcus pneumoniae, Bordetella pertussis, and seasonal influenza decreases, but
does not eliminate, the risk of infection with these organisms

Previous antibiotic therapy

Increases the likelihood of antibiotic-resistant bacteria

Maternal history of chlamydia

during pregnancy (for infants <4
months of age)

May indicate Chlamydia trachomatis infection

Exposure to tuberculosis

May indicate Mycobacterium tuberculosis infection

Ill contacts

More common with viral etiologies

Travel to or residence in certain

areas that suggest endemic

Measles: Developing world

pathogens

Coccidioidomycosis: Southwestern US, northern Mexico, Central and South America

Blastomycosis: Southeastern and central US; states bordering the Great Lakes
Histoplasmosis: Ohio, Missouri, and Mississippi River valleys in the United States; Canada;
Central America; eastern and southern Europe; parts of Africa; eastern Asia; and Australia
Hantavirus: West of the Mississippi River; four corners region of United States (where
borders of Colorado, New Mexico, Arizona, and Utah meet)

Animal exposure

May indicate histoplasmosis, psittacosis, Q fever

Day care center attendance

Exposure to viruses and antibiotic-resistant bacteria

Fluid and nutrition intake

Difficulty or inability to feed suggests severe illness

2013 UpToDate, Inc. All rights reserved. |Subscription and License Agreement|Release: 21.1 - C21.12
Licensed to: Inst Chihuahuense de Salud|Support Tag: [1103-189.254.162.24-A17C8A0CD7-494946.14]