Pneumonia in children: Epidemiology,

pathogenesis, and etiology

Author: William J Barson, MD
Section Editor: Sheldon L Kaplan, MD
Deputy Editor: Diane Blake, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2024. | This topic last updated: Jul 25, 2024.

INTRODUCTION

Childhood pneumonia is an important cause of morbidity in resource-abundant

countries, and morbidity and mortality in resource-limited countries. The
epidemiology, microbiology, and pathogenesis of pneumonia in children will be
reviewed here. The clinical features, diagnosis, and treatment of pneumonia in
children and pneumonia in neonates (<28 days) are discussed separately:
● (See "Community-acquired pneumonia in children: Clinical features and
diagnosis".)
● (See "Community-acquired pneumonia in children: Outpatient treatment".)
● (See "Pneumonia in children: Inpatient treatment".)
● (See "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 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 and hospitalization — The incidence of childhood pneumonia varies

geographically.
● Resource-abundant countries – In resource-abundant countries, the annual
incidence of pneumonia is estimated to be 3.3 per 1000 in children younger than
5 years and 1.45 per 1000 in children 0 to 16 years [1]. Approximately one-half of
children younger than five years of age with community-acquired pneumonia
require hospitalization [2]. Hospitalization rates for pneumonia (all causes)
among children younger than two years in the United States decreased after
introduction of the pneumococcal conjugate vaccine (PCV) to the routine
childhood immunization schedule in 2000 (from 12 to 14 per 1000 population to 8
to 10 per 1000 population between 1997 and 2006) ( figure 1) [3]. After licensure
of 13-valent PCV in 2010, hospitalization rates for pneumonia (all causes) among
children younger than two years in a single state declined to 4 per 1000,
compared with 14 to 15 per 1000 before licensure of the 7-valent PCV (PCV7) and
8 to 9 per 1000 in the PCV7 years [4].
● Resource-limited countries – In a systematic review, the annual incidence of
pneumonia in children younger than five years from resource-limited countries in
2015 was estimated to be 231 per 1000; 50 to 80 percent of children with severe
pneumonia required hospitalization [2].

Mortality — In 2015, lower respiratory tract infections (LRTIs) accounted for nearly
800,000 deaths among children ≤19 years worldwide (31.1 per 100,000 population),
second only to neonatal/preterm birth complications [5]. In observational studies in
resource-abundant countries, the case fatality rate among hospitalized children <5
years of age was <1 percent [2,6]. In a systematic review, the case fatality rate among
hospitalized children <5 years in resource-limited countries ranged from 0.3 to 15
percent [2].

Seasonality — Although both viral and bacterial pneumonia occur throughout the
year, they are more prevalent during the colder months. The mechanisms responsible
for this observed seasonality are likely multifactorial including environmental factors
(eg, temperature, absolute humidity, sunlight) affecting both the pathogen (virus
stability and transmissibility) as well as the host (eg, local, innate, and adaptive
immune function) and human behavior patterns (indoor crowding during the winter
months enhancing direct transmission of infected droplets) [7]. For reasons that are
unknown, different viruses cause peaks of infection at different times during the
respiratory virus season, and these peaks seldom occur simultaneously [8]. In tropical
regions, peaks of infection follow no common pattern and can occur during either the
wet or dry seasons.

Risk factors — 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 caregivers and siblings [8].

Underlying cardiopulmonary disorders and other medical conditions predispose to

pneumonia and contribute to increasing severity. These include [9,10]:
● 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 [11]. 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 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 [12].

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 type b infection", section on 'Efficacy/effectiveness'.)
The universal immunization of infants in the United States and other countries with
the PCV has effectively decreased the incidence of pneumonia requiring
hospitalization and other invasive Streptococcus pneumoniae infections in children
[4,13-17]. (See "Pneumococcal vaccination in children", section on 'Efficacy and
effectiveness'.)

Pneumococcal vaccination also reduces the risk of viral pneumonia. In a randomized

trial, complete immunization with a 9-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 A/B, parainfluenza types 1
to 3, respiratory syncytial virus, 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 [19,20]. The
lower respiratory tract air spaces fill with white blood cells, 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 [19]. Severe infection is associated with necrosis of
bronchial or bronchiolar epithelium [21] and/or pulmonary parenchyma [22].

Acquisition — The agents that cause lower respiratory tract infection 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.

Most typical bacterial pneumonias (eg, S. pneumoniae) 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 (eg, Mycoplasma pneumoniae,
Chlamydia pneumoniae) 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 [23,24], 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 the reference [25].
● Anatomic and mechanical barriers – Anatomic and mechanical barriers in the
upper airway form an important part of the host defense. Particles greater than
10 microns are efficiently filtered by the hairs in the anterior nares or are trapped
on 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
immunoglobulin (Ig)A, 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 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.

Pathologic patterns of pneumonia — There are five pathologic patterns of bacterial

pneumonia [20]:
● 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 ( image 1), S. pyogenes, and S. aureus).
● Caseating granuloma (as in pneumonia caused by Mycobacterium tuberculosis
and the endemic mycoses).
● Interstitial and peribronchiolar with secondary parenchymal infiltration – This
pattern typically occurs when a severe viral pneumonia is complicated by
bacterial pneumonia.

There are two major pathologic patterns of viral pneumonia [20]:

● Interstitial pneumonia ( image 2).
● Parenchymal infection.

ETIOLOGIC AGENTS
A large number of microorganisms have been implicated as etiologic agents of
pneumonia in children ( table 1 and table 2). The agents commonly responsible
vary according to the age of the child and the setting in which the infection is
acquired.

Community-acquired pneumonia — Community-acquired pneumonia (CAP) is an

acute infection of the pulmonary parenchyma that is acquired in the community. The
true prevalence of the various etiologic agents in CAP in children is difficult to
determine. 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 [6,26-37]. Because direct culture of infected lung tissue
requires invasive techniques, published studies primarily use laboratory tests that
provide indirect evidence of etiology (eg, nasopharyngeal culture, blood culture,
polymerase chain reaction (PCR), serology). Interpretation of the results is further
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) [1,6,38].

The most common causes of CAP in children vary with age.

In neonates — The etiology of pneumonia in neonates (infants <28 days of age) is

discussed separately. (See "Neonatal pneumonia", section on 'Etiology'.)

In infants — Viruses are the most common cause of CAP in infants younger than
one year. They account for >80 percent of CAP in children younger than two years [6].
Infants may also develop "afebrile pneumonia of infancy," a syndrome that typically
occurs between two weeks and three to four months of age. 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
"Pertussis infection in infants and children: Clinical features and diagnosis", 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 [1,6,39]. They account for up to 50
percent of cases in young children [6].

Respiratory syncytial virus (RSV), a member of the Pneumoviridae virus family

[40], is the most common viral pathogen responsible for pneumonia in children
younger than five years [6,32,39,41,42]. 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 in infants and children", section on
'Clinical manifestations'.)

Other viral causes of pneumonia in children younger than five years, in

decreasing order of likelihood, include [6,42]:

• Influenza A and B viruses.

• Human metapneumovirus is a common cause of lower respiratory tract
infections (LRTIs) in children; most children have been infected by five years of
age. (See "Human metapneumovirus infections".)

• A number of adenovirus serotypes (eg, 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 [43]. Adenovirus was found to be
strongly associated with CAP in children younger than two years [42]. (See
"Pathogenesis, epidemiology, and clinical manifestations of adenovirus
infection", section on 'Clinical presentation'.)

• Parainfluenza viruses, usually type 3. (See "Parainfluenza viruses in children",

section on 'Clinical presentation'.)

• Enterovirus D68 emerged as a significant pathogen of lower respiratory tract

disease among American children in 2014 [44,45]. (See "Enterovirus and
parechovirus infections: Epidemiology and pathogenesis", section on
'Periodicity and variability of disease by serotype' and "Enterovirus and
parechovirus infections: Clinical features, laboratory diagnosis, treatment, and
prevention", section on 'Respiratory disease'.)

• Coronaviruses (229E, OC43, NL63, HKU1) as well as MERS-CoV (responsible for

Middle East respiratory syndrome) and severe acute respiratory syndrome
 coronavirus 2 (SARS-CoV-2; responsible for coronavirus disease-2019 [COVID-
19]) may also cause respiratory tract infections in children younger than five
years [46-48]. However, their clinical impact has yet to be fully determined
[41,42,49]. (See "Common cold coronaviruses", section on 'Respiratory
syndromes' and "Middle East respiratory syndrome coronavirus: Clinical
manifestations and diagnosis", section on 'Clinical manifestations' and "COVID-
19: Clinical manifestations and diagnosis in children".)

• Rhinovirus has been implicated as a cause of pneumonia using PCR assays on

specimens from the upper respiratory tract [50,51], but its etiologic role is
questioned [6,41,42,52,53], especially in children younger than five years [42].

• Human bocavirus and human parechovirus types 1, 2, and 3 also have been
implicated as causes of LRTIs in children [54-57].
● Bacteria – Important bacterial causes of pneumonia in preschool children include
S. pneumoniae, H. influenzae type b (Hib), nontypeable H. influenzae, Moraxella
catarrhalis, S. aureus, S. pyogenes, and atypical bacteria. S. pneumoniae, S.
aureus, and S. pyogenes are associated with increased morbidity and mortality
[58-60].

• S. pneumoniae is the most common typical bacterial pathogen causing

pneumonia in all patients beyond the first few weeks after birth [10,61]. (See
"Pneumococcal pneumonia in children", section on 'Epidemiology'.)

• Hib is a rare cause of pneumonia in countries with universal childhood

immunization.

• S. aureus (particularly community-associated methicillin-resistant S. aureus

[CA-MRSA]) and S. pyogenes are becoming increasingly frequent causes of CAP,
particularly those complicated by necrosis and empyema [58,62]. In addition,
these organisms occasionally cause pneumonia following influenza and
chickenpox, respectively [59,63]. (See "Epidemiology, clinical presentation, and
evaluation of parapneumonic effusion and empyema in children" and "Clinical
features of varicella-zoster virus infection: Chickenpox".)

When associated with influenza, MRSA CAP can be particularly severe. (See
"Seasonal influenza in children: Clinical features and diagnosis", section on 'S.
 pneumoniae or S. aureus coinfection'.)

• The prevalence of the atypical pathogens M. pneumoniae and C. pneumoniae

may be increasing in preschool children with CAP [64]. (See "Pneumonia
caused by Chlamydia pneumoniae 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 [6,65] (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 [66] (see "Pneumonia caused by Chlamydia
pneumoniae in children")
● Although viruses primarily cause pneumonia in young children, the COVID-19
pandemic has demonstrated that SARS-CoV-2 can be responsible for severe
pneumonia in older children/adolescents who have risk factors such as obesity
(see "COVID-19: Clinical manifestations and diagnosis in children")

In areas where CA-MRSA is prevalent, CA-MRSA is an important cause of CAP

complicated by empyema and necrosis [58,67]. When associated with influenza, MRSA
CAP can be particularly severe [59,63]. (See "Epidemiology, clinical presentation, and
evaluation of parapneumonic effusion and empyema in children" and "Methicillin-
resistant Staphylococcus aureus infections in children: Epidemiology and clinical
spectrum", section on 'Epidemiology and risk factors'.)

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 episodes
of reduced level of consciousness, neurologic disease, dysphagia, gastroesophageal
reflux, alcohol or substance use disorders, use of a nasogastric tube, or foreign body
aspiration.

Hospital-acquired pneumonia — Hospital-acquired pneumonia occurs ≥48 hours

after admission and does not appear to be incubating at the time of admission.
Hospital-acquired bacterial pneumonia is usually caused by gram-negative bacilli or S.
aureus. Hospital-acquired pneumonia frequently occurs in intensive care units where
mechanical ventilation, indwelling catheters, and administration of broad-spectrum
antibiotics are common. (See "Pneumonia in children: Inpatient treatment".)

In addition, during the winter respiratory viral season, hospitalized children are at risk
for hospital-acquired pneumonia caused by RSV, parainfluenza, and influenza viruses.
(See "Seasonal influenza in children: Clinical features and diagnosis" and
"Parainfluenza viruses in children", section on 'Clinical presentation' and "Respiratory
syncytial virus infection: Clinical features and diagnosis in infants and children",
section on 'Transmission and incubation period'.)

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 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 [68,69]. However, seroepidemiologic studies suggest that
subclinical or minor infections occur in children [70,71]. (See "Microbiology,
epidemiology, and pathogenesis of Legionella infection".)

Opportunistic fungi, such as Aspergillus spp, Mucoraceae 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 human immunodeficiency virus (HIV)-infected
patients is Pneumocystis jirovecii, which was formerly called Pneumocystis carinii [72].
(See "Epidemiology and clinical manifestations of invasive aspergillosis" and
"Mycology, pathogenesis, and epidemiology of Fusarium infection" and "Pediatric HIV
infection: Epidemiology, clinical manifestations, and outcome", section on
'Pneumocystis jirovecii pneumonia'.)

Viral causes of pneumonia, which may be life-threatening in the

immunocompromised host, including the post-solid organ and stem cell transplant
populations, include:
● Common community-acquired viral agents such as [73,74]:

• RSV (see "Respiratory syncytial virus infection: Clinical features and diagnosis in
infants and children")

• Adenovirus (see "Pathogenesis, epidemiology, and clinical manifestations of

adenovirus infection")

• Influenza (see "Seasonal influenza in children: Clinical features and diagnosis")

• Parainfluenza (see "Parainfluenza viruses in children", section on 'Risk and
protective factors')

• Rhinovirus (see "Epidemiology, clinical manifestations, and pathogenesis of

rhinovirus infections")

• Human metapneumovirus (see "Human metapneumovirus infections")

● SARS-CoV-2. (See "COVID-19: Clinical manifestations and diagnosis in children".)
● Rubeola (Hecht giant-cell pneumonia). (See "Measles: Clinical manifestations,
diagnosis, treatment, and prevention", section on 'Immunocompromised
patients'.)
● Varicella-zoster virus (VZV). (See "Clinical features of varicella-zoster virus
infection: Chickenpox", section on 'Pneumonia'.)
● CMV. (See "Overview of cytomegalovirus infections in children", section on
'Immunocompromised hosts'.)
 ● Epstein-Barr virus, which may be the trigger for lymphoid interstitial pneumonitis
(LIP), an indolent but progressive process that occurs in children infected with
HIV. LIP can also be seen in patients with common variable immunodeficiency.
(See "Clinical manifestations and treatment of Epstein-Barr virus infection" and
"Classification of diffuse lung disease (interstitial lung disease) in infants and
children", section on 'Disorders of the immunocompromised host'.)

Cystic fibrosis — Young children with cystic fibrosis frequently are infected with S.
aureus, Pseudomonas 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 chronic pulmonary infection".)

Sickle cell disease — The prevalence of pneumonia is increased in children with

sickle cell disease [75]. Atypical bacterial pathogens (eg, M. pneumoniae, C.
pneumoniae) 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 disease include S. pneumoniae associated with functional asplenia, S. aureus, and
H. influenzae [10]. (See "Acute chest syndrome (ACS) in sickle cell disease (adults and
children)", section on 'Common triggers'.)

Environmental considerations

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

endemic pathogens:
● Tuberculosis is most common in immigrants from countries with a high
prevalence of infection (eg, countries throughout Asia, Africa, Latin America, and
eastern Europe) ( figure 2). (See "Epidemiology of tuberculosis".)
● Measles pneumonia is common in the resource-limited countries. (See "Measles:
Clinical manifestations, diagnosis, treatment, and prevention".)
 ● Coccidioides immitis is endemic to the southwestern United States, northern
Mexico, and parts of Central and South America. (See "Primary pulmonary
coccidioidal infection".)
● Blastomyces dermatitidis, causing blastomycosis, is endemic in the southeastern
and central United States and the midwestern states bordering the Great Lakes.
(See "Mycology, pathogenesis, and epidemiology of blastomycosis" and
"Treatment of blastomycosis".)
● In the United States, Histoplasma capsulatum is most common in the Ohio,
Mississippi, and Missouri River valleys but has been identified in all regions
[76,77]. 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 [78]. 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 of the
United States 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".)
● MERS is endemic in countries in or near the Arabian Peninsula. (See "Middle East
respiratory syndrome coronavirus: Virology, pathogenesis, and epidemiology"
and "Middle East respiratory syndrome coronavirus: Clinical manifestations and
diagnosis".)

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:
● Chlamydia psittaci (psittacosis), which is transmitted to humans predominantly
from domestic and wild 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).
Additional information about Q fever is available on the United Stated Centers
for Disease Control and Prevention website [79,80].

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
people experiencing homelessness, recent immigrants from endemic regions
( figure 2), incarcerated individuals, and HIV-infected patients. (See "Epidemiology of
tuberculosis".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and

regions around the world are provided separately. (See "Society guideline links:
Pediatric pneumonia".)

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 6th 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 12th 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 email these topics to your patients. (You can also locate patient
education articles on a variety of subjects by searching on "patient education" and the
keyword[s] of interest.)
● Basics topic (see "Patient education: Pneumonia in children (The Basics)")

SUMMARY
● Epidemiology – 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-age siblings, and underlying
cardiopulmonary and other medical disorders. (See 'Epidemiology' above.)
● Etiology – Pneumonia can be caused by a large number of microorganisms
( table 1 and table 2). 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.)

• Community-acquired pneumonia
- Children <5 years – Viruses are most common. However, bacterial
pathogens, including Streptococcus pneumoniae, Staphylococcus aureus,
and Streptococcus pyogenes, also are important. (See 'In children <5 years'
above.)
- Otherwise healthy children ≥5 years – S. pneumoniae, Mycoplasma
pneumoniae, and Chlamydia pneumoniae are most common. (See 'In
children ≥5 years' above.)
- Children of all ages – Community-associated methicillin-resistant S. aureus
is an increasingly important pathogen.
- Necrotizing pneumonia – Common causes of necrotizing pneumonia
include S. pneumoniae, S. aureus, and S. pyogenes. (See 'Pathologic
patterns of pneumonia' above.)
 • Aspiration pneumonia – Aspiration pneumonia is usually caused by anaerobic
oral flora. (See 'Aspiration pneumonia' above.)

• Hospital-acquired pneumonia – Hospital-acquired pneumonia is usually caused

by gram-negative bacilli or S. aureus. (See 'Hospital-acquired pneumonia'
above.)
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