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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 (

Mortality The mortality rate in developed countries is low (

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

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

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

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

th grade reading level, and

they answer the four or five key questions a patient might have about a given condition. These articles are best for

patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12

th grade reading level

and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to

your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the

keyword(s) of interest.)

Basics topics (see "Patient information: Pneumonia in children (The Basics)")

SUMMARY Pneumonia is more common in children younger than five years of age than in older children and

adolescents. Risk factors for pneumonia include environmental crowding, having school-aged siblings, and underlying

cardiopulmonary and other medical disorders. (See 'Epidemiology' above.)

Pneumonia can be caused by a large number of microorganisms (table 1A-B). The agents commonly responsible vary

according to the age of the child and the setting in which the infection is acquired. (See 'Etiologic agents' above.)

In children younger than five years, viruses are most common. However, bacterial pathogens, including S.

pneumoniae, S. aureus, and S. pyogenes, also are important. (See 'In children

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.)

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Topic 5979 Version 18.0

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

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

* Excluding neonatal pneumonia (in infants

Less common etiologic agents of pediatric pneumonia*

Microbial agent Susceptible hosts

Bacteria

Haemophilus influenzae (typeable and non-

typeable)

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 non-

typeable)

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

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

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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,

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

(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]

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

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

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 (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 is suggestive of pyogenic bacterial disease [58]. However, children with M.

pneumoniae, influenza, or adenovirus pneumonia also may have WBC count >15,000/microL [59-61].

Peripheral eosinophilia may be present in infants with afebrile pneumonia of infancy, typically caused by C.

trachomatis. (See "Chlamydia trachomatis infections in the newborn", section on 'Pneumonia'.)

Acute phase reactants Acute phase reactants, such as the erythrocyte sedimentation rate, C-reactive protein

(CRP), and serum procalcitonin (PCT), need not be routinely measured in fully immunized children with CAP

managed as outpatients [1]. However, for those with more serious disease requiring hospitalization, measurement

of acute phase reactants may provide useful information to assist clinical management.

Measurement of serum CRP may be helpful in distinguishing bacterial from viral pneumonia. A meta-analysis of

eight studies including 1230 patients suggested that children with bacterial pneumonia were more likely to have

serum CRP concentrations greater than 35 to 60 mg/L (3.5 to 6 mg/dL) than children with nonbacterial pneumonia

(odds ratio 2.6, 95% CI 1.2-5.6) [62]. Given a 41 percent prevalence of bacterial pneumonia, the positive

predictive value for CRP values of 40 to 60 mg/L (4 to 6 mg/dL) was 64 percent. An elevated serum PCT

concentration may be as sensitive as but more specific than an increased CRP level for differentiating a bacterial

from a viral process [26,63,64]. However, predictable utility has not been documented [1,65,66].

Acute phase reactants should not be used as the sole determinant to distinguish between viral and bacterial

etiologies of CAP but may be helpful in following the disease course, response to therapy, and in determining

when therapy can be discontinued [1,65,67,68]. (See "Inpatient treatment of pneumonia in children", section on

'Duration of treatment'.)

Serum electrolytes Measurement of serum electrolytes may be helpful in assessing the degree of dehydration in

children with limited fluid intake and whether hyponatremia is present (as pneumonia may be complicated by

SIADH). (See 'Complications' below.)

Microbiology

Indications If possible, a microbiologic diagnosis should be established in children with severe disease (table 3),

potential complications, and those who require hospitalization. Accurate and rapid diagnosis of the responsible pathogen

helps to determine the appropriate antimicrobial therapy [1]. (See "Inpatient treatment of pneumonia in children", section

on 'Overview'.)

A microbiologic diagnosis also should be established if there appears to be a community outbreak [69] or if an unusual

pathogen is suspected, particularly if it requires treatment that differs from standard empiric regimens (eg, S. aureus

including methicillin-resistant strains, Mycobacterium tuberculosis). (See 'Critical microbes' below.)

Children with mild disease who are treated as outpatients usually can be treated empirically, based on age and other

epidemiologic features, without establishing a microbiologic etiology [2,70]. (See "Outpatient treatment of community-

acquired pneumonia in children", section on 'Empiric therapy'.)

Microbiologic diagnosis can be established with culture, rapid diagnostic testing (enzyme immunoassay,

immunofluorescence, polymerase chain reaction [PCR]), or serology.

Cultures

Blood cultures We suggest that blood cultures be performed in children with CAP who require admission to the

hospital and in children with parapneumonic effusion or other complication [1,2,71]. Although blood cultures are

positive in at most 10 to 12 percent of children with pneumonia, when positive they help to confirm the etiologic

diagnosis [72-74]. The yield of blood cultures increases to 30 to 40 percent in patients with a parapneumonic

effusion or empyema [74-76]. The utility of blood culture is limited when antibiotics are administered before

obtaining the specimen. (See "Blood cultures for the detection of bacteremia".)

Blood cultures are not necessary in children with CAP who will be treated as outpatients [1,7,72,77]. In the

outpatient setting, the likelihood of a positive blood culture in children with CAP is less than 3 percent [72,73].

Nasopharyngeal cultures We do not suggest obtaining nasopharyngeal (NP) cultures for etiologic diagnosis in

children with pneumonia. Bacterial organisms recovered from the nasopharynx do not accurately predict the

etiology of pneumonia because bacteria that cause pneumonia also may be normal upper respiratory flora. The

results of NP cultures for viruses and atypical bacterial although helpful may not be available soon enough to

assist with management decisions [7]. Rapid diagnostic tests for viruses and atypical bacteria are discussed

below. (See 'Rapid diagnostic tests' below.)

Sputum cultures We suggest that sputum samples for Gram stain and culture be obtained in children who

require hospital admission if they are able to produce sputum [1]. Children younger than five years usually

swallow sputum, so it is rarely available for examination. Good-quality sputum samples can be obtained by

sputum induction [78]. However, sputum induction is unpleasant and not routinely necessary because most

children respond to empiric antimicrobial therapy. It may be beneficial in children who require intensive-care

therapy, have a pleural effusion, or fail to respond to empiric therapy [78,79]. (See "Inpatient treatment of

pneumonia in children", section on 'Empiric therapy'.)

As a general guide, an appropriate sputum specimen for examination is one with 10 epithelial cells and 25

polymorphonuclear leukocytes (PMN) under low power (x100) [80]. A predominant microorganism and/or

intracellular organisms suggest the etiologic agent. When the following criteria are used, the specificity of the

Gram stain for identifying pneumococci has been shown to be 85 percent, with a sensitivity of 62 percent:

predominant flora or more than 10 Gram-positive, lancet-shaped diplococci per oil immersion field (x1000)

(picture 4) [81].

Pleural fluid cultures Diagnostic (and possibly therapeutic) thoracentesis generally is warranted for children with

more than minimal pleural effusion. Specimens for culture of pleural fluid ideally should be obtained before

administration of antibiotics. The evaluation of pleural fluid is discussed separately. (See "Epidemiology; clinical

presentation; and evaluation of parapneumonic effusion and empyema in children", section on 'Pleural fluid

analysis'.)

Rapid diagnostic tests Rapid diagnostic tests, such as molecular testing using PCR techniques and

immunofluorescence, on NP specimens can be helpful in the management of infants and children who are admitted to the

hospital with probable viral or atypical bacterial CAP. The results of rapid diagnostic tests can be used to make decisions

about treatment and cohorting of patients [1]. The rapid diagnostic tests that are available for the following pathogens are

discussed separately:

Respiratory syncytial virus (see "Respiratory syncytial virus infection: Clinical features and diagnosis", section on

'Diagnosis')

Influenza viruses (see "Clinical features and diagnosis of seasonal influenza in children", section on 'Diagnosis')

Parainfluenza viruses (see "Parainfluenza viruses in children", section on 'Diagnosis')

Adenovirus (see "Diagnosis and treatment of adenovirus infection", section on 'Pneumonia')

M. pneumoniae (see "Mycoplasma pneumoniae infection in children", section on 'Diagnosis')

Chlamydophila spp (see "Pneumonia caused by Chlamydophila (Chlamydia) species in children", section on

'Diagnosis')

Human metapneumovirus (see "Human metapneumovirus infections", section on 'Diagnosis')

Serology We do not suggest routine serologic testing for specific pathogens (eg, S. pneumoniae, M. pneumoniae, C.

pneumoniae) because the results usually do not influence management [7,82,83]. Serologic diagnosis of viral pathogens

is not practical because acute and convalescent specimens are needed. S. pneumoniae has too many potential infecting

serotypes to make antibody determinations practical. Serologic tests for Chlamydophila spp are not readily available.

Although most older children with atypical pneumonia can be treated empirically for M. pneumoniae, serologic and PCR

testing can be helpful in evaluating the younger child. These tests also may be helpful in establishing the diagnosis of M.

pneumoniae in patients with extrapulmonary manifestations, particularly central nervous system manifestations. (See

"Mycoplasma pneumoniae infection in children", section on 'Clinical features'.)

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

include:

Tuberculin skin and interferon gamma release assay if pulmonary tuberculosis is a consideration; additional

diagnostic testing for tuberculosis in children is discussed separately (see "Tuberculosis disease in children",

section on 'Diagnosis')

Urine antigen testing for legionellosis due to serogroup 1 (see "Clinical manifestations and diagnosis of Legionella

infection", section on 'Urinary antigen testing')

Serum and urine antigen testing for histoplasmosis (see "Diagnosis and treatment of pulmonary histoplasmosis",

section on 'Antigen detection')

Urine antigen testing for S. pneumoniae in children should not be performed because of false positive reactions,

some of which may merely indicate colonization with S. pneumoniae [1,2]

Invasive studies Invasive procedures may be necessary to obtain lower respiratory tract specimens for culture and

other studies in children in whom an etiologic diagnosis is necessary and has not been established by other means [1,84-

87]. These procedures are typically reserved for seriously ill patients whose condition is worsening despite empiric

therapy, or individuals with significant comorbidities (eg, immune compromise). They include [1,84-86]:

Bronchoscopy with bronchoalveolar lavage (BAL). Because the accurate identification of bacterial pathogens via

bronchoscopy is hampered by specimen contamination with upper airway normal flora, quantitative culture

techniques are utilized in many centers to differentiate true infection from upper airway contamination [88-90].

Percutaneous needle aspiration of the affected lung tissue guided by computed tomography or ultrasonography.

A small study from Finland found that needle aspiration determined an infectious etiology (21 bacteria and 2

viruses) in 20 of 34 patients (59 percent) studied and in 18 of 26 (69 percent) of those in whom an adequate

specimen was obtained [84]. Six patients developed a pneumothorax, which spontaneously resolved over two to

three days without intervention.

Lung biopsy either by a thoracoscopic or thoracotomy approach. Open biopsy yields diagnostic information that

may affect medical management in up to 90 percent of patients [86]. In one retrospective review, an infectious

etiology was determined by open lung biopsy in 10 of 33 patients with respiratory failure, eight of whom had a

prior nondiagnostic BAL [85]. In another retrospective review, lung biopsy provided a definitive diagnosis in 25 of

50 immunocompromised patients, nine of whom had a prior nondiagnostic BAL [91].

Critical microbes Some microbes are critical to detect because they require treatment that differs from standard

empiric regimens or have public health implications. Diagnostic testing for these pathogens is discussed separately.

Influenza A and B (see "Clinical features and diagnosis of seasonal influenza in children", section on 'Diagnosis')

Community-associated methicillin-resistant S. aureus (see "Treatment of invasive methicillin-resistant

Staphylococcus aureus infection in children", section on 'Pneumonia' and "Epidemiology and clinical spectrum of

methicillin-resistant Staphylococcus aureus infections in children", section on 'Epidemiology and risk factors')

M. tuberculosis (see "Tuberculosis disease in children")

Fungal etiologies (Coccidioides immitis, Blastomyces dermatitidis, Histoplasma capsulatum) (see "Primary

coccidioidal infection" and "Mycology, pathogenesis, and epidemiology of blastomycosis" and "Treatment of

blastomycosis" and "Diagnosis and treatment of pulmonary histoplasmosis")

Legionella species (see "Clinical manifestations and diagnosis of Legionella infection", section on 'Specific

laboratory diagnosis')

Avian influenza (see "Clinical manifestations and diagnosis of avian influenza", section on 'Diagnosis')

Hantavirus (see "Hantavirus cardiopulmonary syndrome")

Agents of bioterrorism (see "Identifying and managing casualties of biological terrorism")

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

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

The diagnostic approach depends, to some extent, upon the setting and the severity of illness. In the appropriate clinical

setting, the diagnosis can be made without radiographs. In children with severe illness, and in those who require hospital

admission, the diagnosis should be confirmed with radiographs. If possible, etiologic diagnosis should be established in

children who require admission to the hospital and in those who fail to respond to initial therapy. (See "Inpatient treatment

of pneumonia in children", section on 'Overview'.)

Clinical diagnosis The diagnosis of pneumonia should be considered in infants and children with respiratory

complaints, particularly cough, tachypnea, retractions, and abnormal lung examination [2,3,7].

The diagnosis of pneumonia can be made clinically in children with fever and historical or physical examination evidence

of an infectious process with symptoms or signs of respiratory distress [7]. Tachypnea, nasal flaring, grunting, retractions,

rales, and decreased breath sounds increase the likelihood of pneumonia [4,9,30,92]. The absence of tachypnea is

helpful in excluding pneumonia; the absence of the other signs is not. (See 'Tachypnea' above.)

In developing countries where there is a high prevalence of pneumonia, the presence of a single positive respiratory sign

increases the certainty of pneumonia [4]. The World Health Organization uses tachypnea (>60 breaths/min in infants 50 breaths/min in infants 2 to 12 months; and >40 breaths/min in children 1 to 5 years; and >20 breaths/min in

children 5 years) as the sole criterion to define pneumonia in children with cough or difficulty breathing [15]. In developed

countries with a lower prevalence of pneumonia, multiple respiratory signs are necessary to increase the certainty of

pneumonia [4,93].

Radiographic confirmation The presence of infiltrates on chest radiograph confirms the diagnosis of pneumonia in

children with compatible clinical findings. Radiographs should be obtained in children in whom the diagnosis is uncertain

and in those with severe, complicated, or recurrent pneumonia [1,2,94]. Radiographic confirmation is not necessary in

children with mild, uncomplicated lower respiratory tract infection who will be treated as outpatients. (See 'Indications'

above.)

Radiographic findings cannot reliably distinguish between bacterial, atypical bacterial, and viral etiologies of pneumonia.

Radiographic findings should be used in conjunction with clinical and microbiologic data to make therapeutic decisions

[2,4]. (See "Outpatient treatment of community-acquired pneumonia in children", section on 'Empiric therapy' and

"Inpatient treatment of pneumonia in children", section on 'Empiric therapy'.)

Etiologic diagnosis The etiologic agent is suggested by host characteristics, clinical presentation, epidemiologic

considerations, and, to some degree, the results of nonspecific laboratory tests and chest radiographic patterns (table 4).

(See 'Clues to etiology' above and 'Etiologic clues' above and "Epidemiology, pathogenesis, and etiology of pneumonia in

children", section on 'Etiologic agents'.)

Specific microbiologic tests can be used to confirm the etiologic diagnosis. Confirmation of etiologic diagnosis is not

necessary in mildly ill patients who can be treated empirically in the outpatient setting. Confirmation of etiologic diagnosis

should be attempted in children who are admitted to the hospital or are suspected to be infected with an unusual

pathogen, or a pathogen that requires treatment that differs from standard empiric regimens, so that therapy can be

directed toward the appropriate pathogen. Etiologic diagnosis also is necessary in children who fail to respond to initial

therapy. (See 'Microbiology' above and 'Critical microbes' above and "Inpatient treatment of pneumonia in children",

section on 'Empiric therapy'.)

DIFFERENTIAL DIAGNOSIS Although pneumonia is highly probable in a child with fever, tachypnea, cough, and

infiltrate(s) on chest radiograph, alternate diagnoses and coincident conditions must be considered in children who fail to

respond to therapy or have an unusual presentation/course [7].

The Table lists a number of other conditions that can mimic an infectious pneumonia (table 5). History and/or associated

clinical features usually help to distinguish the conditions in the table from infectious pneumonia. In some cases,

laboratory studies or additional imaging may be necessary.

Foreign body aspiration must be considered in young children. The aspiration event may not have been witnessed. (See

"Airway foreign bodies in children", section on 'Presentation'.)

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

Bronchiolitis (see "Bronchiolitis in infants and children: Clinical features and diagnosis", section on 'Clinical

features')

Heart failure

Sepsis

Metabolic acidosis (see "Approach to the child with metabolic acidosis", section on 'Clinical evaluation and

diagnosis')

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

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

adults whose illness began with pharyngitis. In Lemierre syndrome, the vessels of the carotid sheath become infected

(typically with Fusobacterium spp), leading to bacteremia and metastatic spread of infection to the lungs and

mediastinum. (See "Suppurative (septic) thrombophlebitis", section on 'Jugular vein'.)

Community-acquired pneumonia (CAP) can be misdiagnosed in young children with asthma who have viral respiratory

infections [96]. Many such children have respiratory distress and may have hypoxemia. The diagnosis of CAP and

treatment with antibiotics must be carefully considered in young children who have a prodrome compatible with a viral

respiratory infection and wheezing, even if there are pulmonary infiltrates (versus atelectasis) on chest radiograph. (See

"Chronic asthma in children younger than 12 years: Evaluation and diagnosis", section on 'Viral URI'.)

Rare, noninfectious lung diseases may present with an intercurrent infectious illness. Pulmonary alveolar proteinosis,

eosinophilic pneumonia, acute interstitial pneumonitis, and cryptogenic organizing pneumonia are entities that should be

considered, especially if the acute illness is atypical or the radiographic and clinical findings do not resolve as expected

with uncomplicated CAP. (See "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults" and

"Idiopathic acute eosinophilic pneumonia" and "Acute interstitial pneumonia (Hamman-Rich syndrome)" and "Cryptogenic

organizing pneumonia".)

COMPLICATIONS Bacterial pneumonias are more likely than atypical bacterial or viral pneumonias to be associated

with complications involving the respiratory tract. Complications of bacterial pneumonia include pleural effusion (image

1A-B), empyema, pneumatoceles, necrotizing pneumonia (image 2), and lung abscesses.

Pleural effusion and empyema The clinical features, evaluation, and management of parapneumonic effusion and

empyema in children are discussed separately. Hypoalbuminemia is common in children with parapneumonic effusions

and hypogammaglobulinemia may be encountered. (See 'Blood tests' above and "Epidemiology; clinical presentation; and

evaluation of parapneumonic effusion and empyema in children" and "Management and prognosis of parapneumonic

effusion and empyema in children".)

Necrotizing pneumonia Necrotizing pneumonia, necrosis, and liquefaction of lung parenchyma, is a serious

complication of community-acquired pneumonia (CAP). Necrotizing pneumonia usually follows pneumonia caused by

particularly virulent bacteria [94]. S. pneumoniae (especially serotype 3 and serogroup 19) is the most common cause of

necrotizing pneumonia (image 2) [97-102]. Necrotizing pneumonia also may occur with S. aureus and group A

streptococcus and has been reported due to M. pneumoniae, Legionella, and Aspergillus. [102-106].

Clinical manifestations of necrotizing pneumonia are similar to those of uncomplicated pneumonia, but they are more

severe [107,108]. Necrotizing pneumonia should be considered in a child with prolonged fever or septic appearance [94].

The diagnosis can be confirmed by chest radiograph (which demonstrates a radiolucent lesion) (image 4) or contrast-

enhanced computed tomography [109]; the findings on chest radiograph may lag behind those of computed tomography

[105].

Pleural effusion/empyema generally accompanies necrotizing pneumonia whereas bronchopleural fistula, pneumatocele,

or abscess formation (which typically is insidious) is much less common. Drainage of the pleural fluid collection is

frequently required but pneumonectomy is rarely needed. (See 'Pneumatocele' below and 'Lung abscess' below.)

Treatment of necrotizing pneumonia is discussed separately. (See "Inpatient treatment of pneumonia in children", section

on 'Complicated CAP'.)

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

necrosis that produces one or more cavities in the lung [44]. Aspiration is the most important predisposing factor for lung

abscess, which may develop one to two weeks after the aspiration event; other predisposing factors include airway

obstruction and congenitally abnormal lung [44]. S. aureus is the organism most frequently involved [95].

Clinical manifestations of lung abscess are nonspecific and similar to those of pneumonia [44]. They include fever, cough,

dyspnea, chest pain, anorexia, hemoptysis, and putrid breath [44,94,110-112]. The course may be indolent.

The diagnosis is suggested by a chest radiograph demonstrating a thick-walled cavity with an air-fluid level (image 4) [44],

and confirmed by contrast-enhanced computed tomography [109]. Lung abscess is often accompanied by parapneumonic

effusion [113,114]. Lung abscess should be suspected when consolidation is unusually persistent, when pneumonia

remains persistently round or mass-like, and when the volume of the involved lobe is increased (as suggested by a

bulging fissure) [44,115].

Interventional radiology may be helpful in obtaining a specimen from the abscess cavity for diagnostic studies. Treatment

of lung abscess is discussed separately. (See "Inpatient treatment of pneumonia in children", section on 'Complicated

CAP'.)

The most common complication of lung abscess is intracavitary hemorrhage. This can cause hemoptysis or spillage of the

abscess contents with spread of infection to other areas of the lung [107]. Other complications of lung abscess include

empyema, bronchopleural fistula, septicemia, cerebral abscess, and inappropriate secretion of antidiuretic hormone [107].

Pneumatocele Pneumatoceles are thin-walled, air-containing cysts of the lungs. They are classically associated with

S. aureus, but may occur with a variety of organisms [116,117]. Pneumatoceles frequently occur in association with

empyema [116]. In most cases, pneumatoceles involute spontaneously, and long-term lung function is normal

[116,118,119]. However, on occasion, pneumatoceles result in pneumothorax [117].

Hyponatremia Hyponatremia (serum sodium concentration 135 meq/L) occurs in approximately 45 percent of

children with CAP and one-third of children hospitalized with CAP, but is usually mild [120-122]. Inappropriate secretion of

antidiuretic hormone (ADH) is the most frequent cause [120,121]. Hyponatremia is associated with increased length of

hospital stay, complications, and mortality. (See "Pathophysiology and etiology of the syndrome of inappropriate

antidiuretic hormone secretion (SIADH)", section on 'Pulmonary disease'.)

INDICATIONS FOR HOSPITALIZATION Indications for hospitalization are discussed separately. (See "Inpatient

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

INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond

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

th grade reading level, and

they answer the four or five key questions a patient might have about a given condition. These articles are best for

patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12

th grade reading level

and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to

your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the

keyword(s) of interest.)

Basics topic (see "Patient information: Pneumonia in children (The Basics)")

SUMMARY AND RECOMMENDATIONS

The presenting signs and symptoms of community-acquired pneumonia (CAP) are nonspecific; no single

symptom or sign is pathognomonic for pneumonia in children. The combination of fever and cough is suggestive

of pneumonia, but the presentation may be subtle, or misleading (eg, abdominal pain or nuchal rigidity). (See

'Clinical presentation' above.)

The history should focus on features that can help to define the clinical syndrome (eg, pneumonia, bronchiolitis)

and narrow the