OVERVIEW: What every practitioner needs to know

Are you sure your patient has community-acquired pneumonia? What are the typical findings for this disease?

The common signs and symptoms associated with pneumonia in children vary by age, responsible pathogen, and severity of the infection. For the majority of children with pneumonia, the triad of fever, cough, and lower respiratory signs are suggestive of pneumonia. Other signs and symptoms depend on the age of the child and are shown in Table I.

Table I:
Common symptoms of CAP in children

Children and infants who have moderate to severe pneumonia should be hospitalized. These include children with respiratory distress and hypoxia (sustained pulse oximetry (SpO2) <90%). Signs of respiratory distress in children are shown in Table II.

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Table II:
Signs of respiratory distress in children with pneumonia

Pneumonia is a clinical condition that results from inflammation of the lung parenchyma. There are many conditions that cause inflammation in the lungs, the most common of which are infections of the respiratory tract. When the inflammation is as a result of an infection acquired in the community, it is referred to as community-acquired pneumonia (CAP).

The definition of pneumonia has been particularly difficult. This is acutely so in young children where bronchiolitis and pneumonia are common and have similar clinical findings.

Some studies describing pneumonia have relied solely on clinical signs and symptoms, while other have included the presence of infiltrates on chest radiographs to define pneumonia.

For the purpose of this chapter, acute pneumonia is defined as an acute lower respiratory tract infection with fever, the presence of lower respiratory signs (Table II) and the presence of radiographic changes in one or both lungs on a chest radiograph.

What other disease/condition shares some of these symptoms?


– Atelectasis (mucous plug, foreign body)

– Bronchiolitis/bronchitis

– Reactive airway disease/asthma

– Aspiration syndromes (gastroesophageal reflux, tracheoesophageal fistula, cleft palate, neuromuscular disorders)

– Lung abscess

– Parapneumonic effusions

– Congenital lung malformations (sequestered lobe of the lung, pulmonary agenesis and hypoplasia, cystic adenomatoid malformation (CAM), bronchogenic cyst, and other lung cysts)

– Pulmonary embolism

– Bronchiectasis

– Cystic fibrosis

– Tuberculosis


– Pulmonary edema from congestive heart failure

– Vascular ring


– Sepsis and adult respiratory distress syndrome (ADRS)

– Vasculitic syndromes (Wegener’s granulomatosis, systemic lupus erythematosus, juvenile rheumatoid arthritis)

– Drug-induced pneumonitis (Nitrofurantoin, Bleomycin, cytotoxic drugs, opiates)

– Radiation therapy

– Smoke inhalation

– Lipoid pneumonias

What caused this disease to develop at this time?

Pneumonia develops when the normal defense mechanism (anatomic and mechanical barriers, humoral immunity, phagocytic activity, and cell-mediated immunity) in the lower respiratory tract are disrupted or impaired, and overwhelmed by viruses or bacteria in the lower airways.

The normal defense mechanisms are disrupted most commonly by respiratory viral infections, but also by chemical irritants and environmental pollutants. With impaired clearance of viruses and bacteria in the lower respiratory tract, proliferation of bacteria in alveoli triggers an immune and inflammatory response.

As a result, there is alveolar congestion, WBC infiltration, alveolar edema, and deposition of cellular debris in the alveoli. This decreases lung compliance, collapse of alveoli and lung ventilation-perfusion mismatch giving rise to the signs and symptoms of CAP.

What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?

Microbiologic testing

Blood culture:

-Blood cultures are recommended for all children hospitalized with presumed bacterial CAP.

-Blood cultures are positive in less than 3% of children hospitalized with CAP, but higher (~20%) in children with parapneumonic effusion/empyema.

Respiratory bacterial culture:

-Gram stain and culture of expectorated sputum should be attempted in children up to 8 years of age with severe disease, failure of outpatient therapy, and intensive care unit admission.

-An appropriate sputum specimen for testing has less than 10 epithelial cells and over 25 polymorphonuclear leukocytes (PMN) under low power (x100).

-For children admitted to intensive care with CAP, respiratory samples collected from the endotracheal tube using a suction catheter and specimen trap, standard protected specimen brush or bronchoalveolar lavage is recommended for gram stain, bacterial culture, and respiratory viral testing.

Testing for viral pathogens:

Testing for rhinovirus, respiratory synctial virus (RSV), influenza A and B (Inf A & B), adenovirus, parainfluenza virus, or human metapneumovirus (hMPV) or human coronavirus (HCoV) from respiratory specimens (nasopharyngeal, oropharyngeal, or tracheal) by rapid respiratory viral testing (RSV and Inf A & B), direct fluorescent antibody testing or by the more sensitive polymerase chain reaction (PCR) is recommended for all children hospitalized with CAP.

Ancillary testing

Complete blood count:

-Complete blood count with white blood cell (WBC) and differential count results may influence therapy in hospitalized children with CAP.

-WBC count alone is poor at making the diagnosis of bacterial pneumonia, but is elevated in many children with bacterial pneumonia.

-The degree of elevation does not reliably distinguish bacterial from viral infection.

WBC and differential count consideration in the evaluation of CAP include:

– WBC <15,000/μL suggests a nonbacterial etiology. However, neutropenic and severely ill patients may have low WBC.

– WBC >15,000/μL is suggestive of bacterial disease. However, children with M. pneumoniae, influenza, or adenovirus may have WBC >15,000/μL.

– Peripheral eosinophilia in infants with afebrile pneumonia of young infants is suggestive of Chlamydia trachomatis.

– Anemia and or thrombocytopenia may raise suspicions for hemolytic-uremic syndrome, which may occur with pneumococcal pneumonia and influenza infection.

Acute phase reactants:

Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin (PCT) do not reliably distinguish bacterial from viral infections when used as the only diagnostic test.

There is a wide variation in CRP and ESR values between children with CAP attributable to bacteria and viruses, whose values did not differ significantly between the two groups.

PCT, while promising, is limited in distinguishing non-serious bacterial from viral pneumonia in children because the values are widely distributed. However, low values may be helpful in distinguishing viral pneumonia from bacterial pneumonia associated with bacteremia.

Declining values of CRP or PCT may correlate with improvement in clinical symptoms and thus have the potential to serve as objective measures of disease resolution.

Testing for atypical bacteria

M. pneumoniae:

Testing is recommended in children with a high likelihood of M. pneumoniae infection, e.g. children failing antibacterial therapy and older children.

Serum IgM and/or IgG by enzyme-linked immunoassays may be helpful; however, because of delays in the immunoglobulin response to infection, testing may not be useful in the acute care setting.

PCR of naso- and oro-pharyneal (NP/OP) samples is more sensitive. However, the availability of PCR testing in some hospitals may be limited.

C. pneumoniae:

Serum IgM and/or IgG by enzyme immunoassays or microimmunofluorescence.

Testing may not be useful in the acute setting of CAP, but a four-fold increase in immunoglobulin during convalescence is helpful.

Pleural fluid evaluation:

White blood cell count and differential count, pH, glucose, protein, and lactate dehydrogenase are useful in distinguishing a transudative from an exudative effusion, however they may not change patient management.

Gram stain and bacterial culture of pleural fluid are recommended to identify the responsible pathogen and direct antibiotic therapy.

Would imaging studies be helpful? If so, which ones?

Imaging studies:

-Supine anteroposterior (young children) or upright posteroanterior chest view (up to 4 years).

-An upright lateral view may be needed to evaluate the retro-cardiac pneumonia, which may be obscured by the heart.

-Lateral decubitus view to evaluate pleural effusion (affected side down).

-Chest ultrasound or computed tomography (CT) is useful in defining the anatomy of pleural space in cases of suspected complicated parapneumonic effusion.

Etiologic considerations:

Infections with bacteria, atypical bacteria, or respiratory viruses are associated with certain radiographic features. However, none reliably differentiate between a bacterial, atypical bacterial, and viral pneumonia.

Segmental consolidation often indicates bacterial pneumonia but lacks sensitivity. However, radiographic features of segmental collapse (atelectasis), a common feature in bronchiolitis, are not always easy to distinguish from segmental consolidation.

A lobar infiltrate suggests a pyogenic bacterial etiology. Most but not all lobar pneumonias are pneumococcal. Single-lobe involvement may also be seen in patients with M. pneumoniae pneumonia.

Consolidative lobar infiltrate in the presence of a large pleural effusion or parenchymal necrosis is highly suggestive of a bacterial etiology.

Spherical or round consolidation pneumonia are seen in young children. Round pneumonias tend to be up to 3cm, located posterior and are solitary. Round pneumonias are commonly associated with S. pneumoniae, but seen with other streptococci, H. influenzae, staphylococci, and M. pneumoniae infection.

Lung pneumatoceles, cavitation, and necrotizing processes are suggestive of a bacterial infection.

Bronchopneumonia has frequently been described with M. pneumoniae and respiratory viral infection. Certain S. pneumoniae serotypes (6, 18, and 19) have been associated with a similar radiographic pattern in children.

Interstitial pneumonia, or diffuse bilateral interstitial inflammatory infiltrates, are typically associated with viral pneumonia, Pneumocystis jirovecii and M. pneumoniae.

In radiologically-confirmed CAP, radiologic abnormalities lag behind clinical resolution by 3 to 6 weeks, with persistent and residual abnormalities in 10% to 30% of children. Serial imaging is not helpful in a patient who is improving clinically.

Confirming the diagnosis

The indication for and modes of pleural fluid drainage in children with parapneumonic effusion and empyema is shown in Figure 1.

Figure 1.
Management of children with parapneumonic effusion.

If you are able to confirm that the patient has community-acquired pneumonia, what treatment should be initiated?

Supportive therapy

Oxygen therapy and ventilator support:

-Hospitalized children with CAP should be monitored with continuous pulse oximetry and blood gas carbon dioxide and oxygen if indicated.

-Hypoxic children (SpO2) <90%) should receive supplemental oxygen, and if in respiratory failure, managed appropriately in intensive care.

Fluid therapy:

-Fever, tachypnea, and poor feeding in children increase insensible fluid loss in children with CAP. Hydration should be maintained in non-critically ill children with oral fluids and intravenously if unable to tolerate fluids.

Fever and pain management:

-Fever increases metabolic oxygen consumption and chest pain from pleurisy may result in shallow breathing and impair effective coughing. Antipyretic and analgesic agents are recommended to make the child comfortable.

Chest physiotherapy:

-Has no role in the management of hospitalized CAP in children.


In children, respiratory viruses are the cause of the majority of hospitalized CAP, and antibiotics are not indicated in the management of CAP caused by respiratory viruses. Antibiotics should be administered if the history, physical examination, and laboratory data are suggestive of a bacterial component.

The initial choice of antibiotic therapy depends on a number of factors. These include the age of the child, the likely pathogens and resistance patterns, route of administration, tolerability of the antimicrobial, as well as its cost.

Etiologic considerations and treatment options

Viral origin:

1. Consider in all children, especially those under 5 years.

2. History of, or ongoing, upper respiratory tract infection.

3. Diffuse and bilateral findings on auscultation of the chest.

4. Non-focal with interstitial distribution on a chest radiograph.


With the exception of infection with influenza virus, the majority of hospitalized CAP caused by respiratory viruses are managed with supportive therapy (above) and do not require antibiotic therapy. However, one should consider antibiotics if chest radiographs show a lobar infiltrate. Children hospitalized with influenza-associated pneumonia should be treated with antivirals. Agents and duration of therapy recommended for the treatment of CAP are shown in Table III and Table IV.

Table III:
Influenza antiviral therapy

Table IV:
Empiric therapy for hospitalized pediatric CAP

Bacterial origin:

1. Consider in all groups.

2. History of chills and rigors or presentation with clinical sepsis.

3. Elevated WBC, immature neutrophils, CRP, and ESR.

4. Focal findings on auscultation of the chest.

5. Focal alveolar infiltrate, lobar consolidation with or without a parapneumonic effusion, pneumatoceles, necrotizing lung or cavitation.


S. pneumoniae remains the most common cause of CAP in all children, even during the pneumococcal conjugate vaccine (PCV) era.

Other bacteria such as group A streptococcus, S. aureus, H. influenzae type B (unimmunized), and other Streptococcus spp. should be considered in selecting antibiotic therapy in hospitalized children with CAP.

Community-associated methicillin-resistant S. aureus (CA-MRSA) is an increasing problem in many areas of the U.S., and comprises more than 50% to 70% of S. aureus isolates in some regions. Pneumonia suspected to be caused by S. aureus should initially be treated in an inpatient setting. Recommended intravenous and oral antibiotics are shown in Table IV, Table V, and Table VI.

Table V:
Antibacterial therapy (parenteral)

Table VI:
Antibacterial therapy (oral)

Consider antibiotic therapy with:

– Ampicillin or penicillin G in a fully-immunized infant or school-aged child, and in locales where the prevalence of high-level penicillin-resistance is low among invasive S. pneumoniae.

– A third-generation parenteral cephalosporin, e.g. ceftriaxone or cefotaxime, in infants and children who are not fully immunized, in locales where the prevalence of high-level penicillin-resistance is high among invasive S. pneumoniae, or for infants and children with life-threatening infection, including those with empyema.

– A macrolide (oral or parenteral) in addition to a beta-lactam antibiotic should be considered for a child hospitalized with CAP in whom M. pneumoniae or C. pneumoniae significant considerations (i.e., up to 5 years of age).

– Vancomycin or clindamycin should be added to beta-lactam therapy if clinical, laboratory, or imaging characteristics are consistent with infection caused by S. aureus until MRSA can be excluded.

– Third-generation cephalosporins (cefotaxime, ceftriaxone) may be more appropriate for young children (under 1 year) and for children of all ages with more severe illness as they cover a broader range of pathogens, including penicillin-resistant S. pneumoniae.

Antibiotics for 10 days (combined intravenous and/or oral) are recommended for the treatment of uncomplicated CAP for most bacteria. Infection with CA-MRSA may require longer treatment.

Intravenous therapy may be transitioned to oral therapy with clinical improvement (no fever for 48 hours and able to tolerate oral medication).

If a pathogen is identified from blood culture or culture of an appropriately collected respiratory tract specimen, appropriate narrow-spectrum antibiotics should be considered for the completion of therapy.

Atypical bacterial origin:

1. Consider in all children, especially those older than 5 years or any child who has failed to respond to antibacterial therapy.

2. Non-specific systemic symptoms including sub-acute onset, sever sore throat, myalgia, malaise, headache, and conjunctivitis.

3. Diffuse and bilateral findings with wheezing on auscultation of the chest.

4. Non-focal and extensive interstitial distribution on a chest radiograph.


Atypical bacteria that cause CAP include C. trachomatis in young infants, and M. pneumoniae and C. pneumoniae in older children and adolescents. Recommended empiric intravenous and oral antibiotics are shown in Table IV, Table V, and Table VI.

A 5 to 10 day course of a macrolide (azithromycin, erythromcyin) antibiotic is adequate to treat uncomplicated CAP caused by atypical bacteria.

What are the adverse effects associated with each treatment option?


Adverse drug reactions to antibiotics do occur with varying frequency. Drug-related adverse events associated with systemic antibiotics in the United States account for approximately 19% of emergency department (ED) visits, of which 78% are allergic reactions.

Allergic reactions (urticaria, eosinophilia) to penicillins and cephalosporins are the most commonly reported adverse events. Others include antibiotic-associated diarrhea and Clostridium difficile colitis (all antibiotics), neutropenia (penicillins and cephalosporins) and thrombophlebitis (penicillins).

Line infections have been associated with percutaneous central catheters and phlebitis with peripheral intravenous catheters.

Chest tube placement with and without fibrinolysis:

-Pain and hemorrhage with chest tube placement.

-Fibrinolytic therapy (tissue plasminogen activator or urokinase) may cause pleural hemorrhage after prolonged use (over 3 days).

Videoscopic-assisted thoracoscopy (VATS):

-Pain and hemorrhage and risks associated with general anesthesia.

What are the possible outcomes of community-acquired pneumonia?

The majority of children with hospitalized bacterial or viral CAP recover without any sequelae.

Bacterial pneumonias are more commonly associated with complications than atypical bacterial or viral pneumonias.

Complications of bacterial pneumonia include: bacteremia, pleural effusion, pneumatoceles, necrotizing pneumonia, lung abscesses, and rarely, pneumococcal hemolytic uremic syndrome.

Necrotizing pneumonia and lung abscess:

Necrotizing pneumonia results from a focal area of necrosis and liquefaction of lung parenchyma. With secondary bacterial infection, necrotizing pneumonia progresses to a lung abscess. Lung abscesses also develop after aspiration of infected oral secretions, septic emboli, and chronic airway infection (e.g., bronchiectasis).

Pathogens frequently isolated include S. pneumoniae (serotype 3 and 19a), S. aureus (especially CA-MRSA), and group A streptococcus. Rarely, M. pneumoniae cause lung necrosis.

Pathogens associated with lung abscesses following aspiration include: anaerobic streptococci, Fusobacterium species, Peptostreptococcus species, Bacteroides species, and Prevotella species.

The clinical manifestations of necrotizing pneumonia and lung abscesses are similar to, but more severe than, those of uncomplicated pneumonia. It should be considered in a child with CAP and prolonged fever despite appropriate antibiotic therapy. Persistently elevated ESR or CRP and thrombocytosis suggest lung necrosis or abscess.

The diagnosis is suggested by a chest radiograph which demonstrates a radiolucent lesion in the case of necrotizing lung or a thick-walled cavity with an air-fluid level, and confirmed by contrast-enhanced CT.


Consider parenteral therapy with a penicillin or third-generation cephalosporin and clindamycin. In locales with high rates of CA-MRSA or in patients requiring intensive care admission, vancomycin or linezolid should be added to therapy (See Table V).

The treatment usually includes a course of antibiotics for approximately 4 weeks or 2 weeks after the patient becomes afebrile, and the patient demonstrates clinical improvement.

In cases of a lung abscess up to 4 cm in diameter, percutaneous drainage by interventional radiology or by surgery may be required.

Abscess samples when available should undergo diagnostic testing by staining and culture (bacteria, fungi, and acid fast bacilli).

Parapneumonic effusion/empyema:

Parapneumonic effusion develops from increased fluid leakage into the pleural space from the visceral pleura overlying the pneumonia. The pleural fluid (PF) initially is sterile with a low leukocyte count. With time, bacteria invade the fluid, resulting in empyema, which is defined as the presence of grossly purulent fluid (>50,000 white blood cells/μL) in the pleural cavity, or positive bacterial culture of pleural fluid.

Parapneumonic effusion progresses in three loosely defined stages:

1. Exudative stage: in this first stage, the PF exudate is simple and uncomplicated, characterized by normal glucose concentration, normal pH, and a low cell count. The PF layers out on decubitus chest radiographs.

2. Fibrinopurulent stage: in this stage, there is accumulation of neutrophils in the PF, bacterial invasion and fibrin deposition on the pleural surfaces and the formation of loculations in the pleural space. This makes drainage difficult. During this stage, pH and glucose concentration decrease and lactate dehydrogenase (LDH) concentrations increase in PF. PF in the fibrinopurulent stage are sometimes labeled complicated pleural effusions. Loculated pleural effusions usually do not layer out on decubitus radiographs.

3. Organizational stage: in this stage, fibroblasts grow on both parietal and visceral pleural surfaces, forming an inelastic “pleural peel” that restricts lung re-expansion and impairs lung function. This stage typically occurs 2 to 4 weeks after initial development of the empyema.

With the introduction of conjugate seven-valent S. pneumoniae vaccine (PCV7) in 2000, there were increases in cases of parapneumonic effusion/empyema in the United States, despite a decrease in cases of pneumonia. Non-PCV7 S. pneumoniae serotypes (serotypes 1, 3, 7F and 19A) were the most common cause of empyema in the PCV7 era. CA-MRSA, group A streptococcus, Streptococcus spp. and Fusobacterium spp. have also been isolated from children with empyema.

In regions of the world, including the United States, where PCV13 replaced PCV7, cases of parapneumonic effusion/empyema have declined, with ongoing pneumococcal effusion/empyema caused by serotype 3.


S. pneumoniae remains the most commonly isolated pathogen by culture and in culture-negative empyema by PCR. However, S. aureus and group A streptococcus continue to remain important causes of empyema.

The choice of initial antibiotic should be directed by regional epidemiology of common causes of CAP. The antibiotic treatment of parapneumonic effusion/empyema is similar to that for CAP without effusion (See Table IV, Table V, Table VI). Most experts recommend empiric therapy with a third-generation cephalosporin and clindamycin. Consider the addition of vancomycin or linezolid to therapy in locales with high rates of clindamycin resistance among CA-MRSA or intensive care admission.

The indication for and modes of pleural fluid drainage are shown in Figure 1. The choice of drainage of PF depends upon the experience and expertise available in the hospital.

A summary of fibrinolytic regimens are shown in Table VII.

Table VII:
Dose and frequency of fibrinolytic regimens

The optimal duration of antibiotic treatment of parapneumonic effusion/empyema depends on the adequacy of the drainage procedure, and pathogen isolated. Experts commonly recommend antibiotics for 4 weeks or for 2 weeks following the resolution of fever; however, the optimal duration is not known.

What causes community-acquired pneumonia and how frequent is it?


In the United States, CAP remains one of the most common causes of outpatient healthcare visits and hospitalization, and is the 8th leading cause of death in children.

Hospitalization rates for CAP (all causes) among children younger than 2 years in the United States decreased following introduction of the PCV7 to the routine childhood immunization schedule in 2000 and switch to PCV13 in 2010. The incidence of pneumonia and risk of severe pneumonia are greater in infants and young children.

The incidence rates of hospitalized CAP among children in the United States from 2010 through 2012 are:

– <2 years: 62.5 per 10,000 children per year

– 2 to 4 years: 23.8 per 10,000 children per year

– 5 to 9 years: 10.1 per 10,000 children per year

– 10 to 17 years: 4.2 per 10,000 children per year

Respiratory viruses

Respiratory viruses are the most common cause of CAP in children. They are isolated in up to 80% of children younger than 5 years and hospitalized with CAP, and less frequently in older children.

Respiratory syncytial virus (RSV) is the most common and is detected in up to 40% of young children (younger than 5 years) with a positive respiratory viral test.

Rhinovirus is the second most common and is detected in up to 25% of young children with a positive respiratory viral test.

Less frequently, influenza A and B viruses, human metapneumovirus, parainfluenza viruses, rhinovirus, adenoviruses, and coronaviruses cause CAP in children.

Recently, human bocavirus and parechovirus have been isolated in children with lower respiratory tract infection.

Concurrent infection with 2 or more viruses occurs in 2% to 33% of children hospitalized with CAP.

Bacteria (typical and atypical)

Bacteria responsible for hospitalized CAP in children vary by age. In children under 5 years of age, bacteria associated with CAP include: S. pneumoniae, non-typeable H. influenzae, Moraxella catarrhalis, S. aureus, and group A streptococcus. In the PCV7 era, non-PCV7 S. pneumoniae serotypes remain the most common bacterial cause of CAP in children.

S. aureus, especially CA-MRSA, have increasingly been isolated in cases of complicated pneumonia in the United States.

In children over 5 years of age, S. pneumoniae remains a common cause of hospitalized CAP, with S. pyogenes and CA-MRSA.

M. pneumoniae is the most common (8%) atypical bacteria isolated from children hospitalized with CAP. Itaccounted for a steadily increasing proportion of pneumonia with increasing age; 3% in children younger than 5 years and 18% in children 5- to 17 years of age.

What complications might you expect from the disease or treatment of the disease?

Complications associated with CAP include:

1. Pulmonary:

– Parapneumonia effusion/empyema

– Necrotizing pneumonia

– Lung abscess

– Acute respiratory failure

– Pneumothorax

2. Metastatic:

– Central nervous system infection (e.g., brain abscess, meningitis)

– Cardiovascular system infection (e.g., endocarditis, pericarditis)

– Musculoskeletal system infection (e.g., osteomyelitis, septic arthritis)

3. Systemic:

– Sepsis / systemic inflammatory response syndrome

– Hemolytic uremic syndrome

Are additional laboratory studies available; even some that are not widely available?

In cases of culture-negative parapneumonic effusion/empyema, S. pneumoniae antigen testing of pleural fluid is useful identifying cases caused by S. pneumoniae.

Nucleic acid amplification by polymerase chain reaction increases pathogen detection in pleural fluid. This has the advantage of detecting a number of different pathogens (e.g., group A streptococcus, H. influenzae, M. pneumoniae, non-pneumococcal streptococcus species and Fusobacterium species), in both culture-positive and culture-negative parapneumonic effusion/empyema.

How can community-acquired pneumonia be prevented?

Not all people with risk factors will get pneumonia, but the risk of pneumonia in children can be decreased by:

– Immunization against S. pneumoniae and H. influenzae type B.

– Annual immunization against influenza virus in all children ( over 6 months) and adolescents.

– Immunization of caretakers of infants less than 6 months of age, including pregnant adolescents, with influenza virus and pertussis vaccines to protect the infants from exposure.

– Infants at high-risk of severe respiratory synctial virus (RSV) infection should receive RSV-specific monoclonal antibody prophylaxis according to American Academy of Pediatrics guidelines.