Download Pneumococcal pneumonia in children Authors: Elaine I Tuomanen

Pneumococcal pneumonia in children
Authors:
Elaine I Tuomanen, MD
Sheldon L Kaplan, MD
Section Editor:
Morven S Edwards, MD
Deputy Editor:
Mary M Torchia, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2016. | This topic last updated: Oct 16, 2015.
INTRODUCTION — Pneumococcus (Streptococcus pneumoniae) is a common cause of invasive bacterial infection
in children and a frequent cause of community-acquired pneumonia (CAP) [1,2]. Intermediate or high-level resistance
to penicillin has become a significant problem. Children, particularly those in child care facilities and those receiving
frequent courses of antibiotics, appear to be important carriers of resistant strains [3-5].
The clinical features, diagnosis, and treatment of pneumococcal pneumonia will be reviewed here. An overview of the
clinical features and diagnosis of CAP in children and the microbiology, pathogenesis, and epidemiology of S.
pneumoniae are discussed separately. (See "Community-acquired pneumonia in children: Clinical features and
diagnosis" and "Microbiology and pathogenesis of Streptococcus pneumoniae".)
PATHOGENESIS — The pneumococcus is acquired by aerosol or inhalation, leading to colonization of the
nasopharynx; pneumococci are carried asymptomatically in approximately 50 percent of individuals at any point in
time [6]. In children, the incidence of pneumococcal carriage may be as high as 60 percent, even after immunization
with the pneumococcal conjugate vaccine [7-9] (see "Microbiology and pathogenesis of Streptococcus pneumoniae",
section on 'Pathogenesis'). Antibiotic-resistant strains are increasingly common [10]. (See "Resistance of
Streptococcus pneumoniae to beta-lactam antibiotics" and "Resistance of Streptococcus pneumoniae to the
fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole" and"Resistance of Streptococcus pneumoniae to
the macrolides, azalides, lincosamines, and ketolides".)
Invasive disease most commonly occurs upon acquisition of a new serotype, typically after an incubation period of
one to three days.
The incidence of disease increases strongly in association with a viral illness, such as influenza, parainfluenza,
respiratory syncytial virus, adenovirus, or human metapneumovirus [11-14]. In a case-control study, upper respiratory
infections with viruses such as influenza and parainfluenza correlated with acquisition of new serotypes of
pneumococci in children [15]. This association is believed to be related to increased expression of receptors for
pneumococcal attachment on virally activated respiratory epithelial cells [16]. In addition, viral neuraminidases cleave
sialic acid from host cell glycoconjugates, and the resulting free sugar is used as a nutrient to increase the growth
and density of pneumococci in the nasopharynx [17]. This adds another dimension to the synergy between viruses
and pneumococci in the pathogenesis of pneumonia.
Pneumococci are presumably aerosolized from the nasopharynx to the alveolus, where they enter alveolar type II
cells. This invasive process involves bacterial binding to the receptor for platelet activating factor (PAF), a key
pulmonary chemokine [18]. The binding occurs via choline, a chemical constituent shared between the surface of the
bacteria and PAF. Choline is present on the surfaces of many pulmonary pathogens, suggesting a common
mechanism for pulmonary infection [19]. The innate host C-reactive protein binds to choline and opsonizes pathogens
that pass from the lungs into the bloodstream. Thus, although choline is useful in the organism's binding to the lung, it
is detrimental to the organism in the bloodstream. (See "Microbiology and pathogenesis of Streptococcus
pneumoniae", section on 'Pathogenesis'.)
The pneumonic lesion progresses as pneumococci multiply in the alveolus and invade the alveolar epithelium.
Pneumococci pass from alveolus to alveolus through the pores of Cohn, thereby creating inflammation and
consolidation strictly along lobar compartments. The center of the spreading lesion shows more advanced
inflammation than do the edges.
The evolution of lung consolidation is as follows [20]:
●Newly involved regions demonstrate engorgement of alveolar capillaries with frothy, serous, blood-tinged fluid
in the alveolar spaces. This lesion can be recapitulated by instillation of heat-killed pneumococci into the lung
and, therefore, may result from host response to the pneumococcal cell wall [21].
●Engorgement of alveolar capillaries rapidly progresses to red hepatization, characterized by a dry, granular,
dark red lung surface and alveoli filled with copious, clotted inflammatory exudate. A distinctive feature of the
exudate is its "freshness" in that erythrocytes and leukocytes are intact, and a fibrin network extends from one
alveolus into the next through the pores of Cohn. Pneumococci are intact and alive. Bronchoalveolar lavage
fluid contains large amounts of tumor necrosis factor, interleukin-6, and nitric oxide reflective of strong
recruitment of leukocytes to the infected focus [22]. However, little tissue destruction or necrosis occurs during
this process, perhaps explaining why the patient and lung architecture may recover fully from these lesions.
●As red hepatization progresses over two to three days, leukocytes pack into the alveoli, erythrocytes are
lysed, and epithelial cells degenerate, leading to grey hepatization. Dying pneumococci release the poreforming toxin pneumolysin, which contributes to this damage.
●In the presence of antibody, pneumococci are opsonized and then phagocytosed by leukocytes and begin to
be cleared. Consolidation remains prominent after defervescence. An abrupt disappearance of fever, termed
"crisis," is particularly common in children. Resolution results in a jelly-like consistency to the lung with a slimy,
yellowish exudate. The involvement of mononuclear cells in the exudate is characteristic of this stage.
Absorption of the exudate is remarkably efficient, with little organization or permanent scarring.
EPIDEMIOLOGY
Burden of disease — Pneumonia is the single most common disease causing death in children worldwide [23].
Community-acquired pneumonia (CAP) can be caused by a variety of bacterial and viral pathogens, and the
predominant pathogen varies depending on age. Overall, S. pneumoniae is the most common cause of CAP,
although in many cases an organism cannot be isolated. The burden of pneumococcal pneumonia in children
declined after the 7-valent pneumococcal conjugate vaccine (PCV7) was replaced with the 13-valent pneumococcal
conjugate (PCV13) vaccine in 2010 [24]. (See "Pneumonia in children: Epidemiology, pathogenesis, and etiology",
section on 'Community-acquired pneumonia'.)
Serotypes — The pneumococcal serotypes isolated from children with pneumococcal pneumonia have changed
since the addition of PCV7 (table 1) to the routine childhood immunization schedule in the United States. In the prePCV7 era, serotypes 6B, 14, and 19F were the most frequently isolated in both complicated and uncomplicated
disease [25,26]. Following introduction of PCV7 in 2000, serotypes not included in PCV7, including serotypes 1, 3, 5,
7F, 12, and 19A, were more frequently isolated, particularly from children with complicated pneumonia [27-32].
PCV13, which contains all of these serotypes except 12, replaced PCV7 in 2010. During 2011 surveillance for
invasive pneumococcal infections at eight children's hospitals in the United States, serotypes 19A and 7F remained
the most common serotypes isolated from children hospitalized with pneumonia [33]. In another study, serotype 3
was isolated from pleural fluid specimens in 15 of 20 children with pneumococcal empyema, one-third of whom had
received PCV13 [34]. (See "Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children", section on
'13-valent vaccine' and 'Effusion/empyema' below.)
Risk factors — Risk factors for invasive pneumococcal disease are listed in the table (table 2).
Antibiotic resistance — Resistance of S. pneumoniae to multiple antibiotics is an increasingly important clinical
problem. A discussion of pneumococcal drug resistance is presented separately. (See "Resistance of Streptococcus
pneumoniae to beta-lactam antibiotics" and "Resistance of Streptococcus pneumoniae to the macrolides, azalides,
lincosamines, and ketolides" and "Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and
trimethoprim-sulfamethoxazole".)
CLINICAL FEATURES
Transmission and incubation period — S. pneumoniae is transmitted from person to person through contact with
respiratory droplets [2]. The period of communicability is not known but is probably less than 24 hours after initiation
of appropriate antimicrobial therapy. The incubation period depends upon the type of infection, but may be as short
as one to three days [2].
Clinical manifestations — Pneumococcal pneumonia is the paradigm of classic lobar bacterial pneumonia [20]. The
most common clinical signs and symptoms are fever, nonproductive cough, tachypnea, and decreased breath sounds
over the affected area. Auscultatory findings of crepitant rales (crackles) and tubular breath sounds are highly
localized to the involved segment or lobe. These findings may disappear at the height of consolidation and reappear
on resolution (redux crepitus). (See "Community-acquired pneumonia in children: Clinical features and diagnosis",
section on 'Clues to etiology'.)
In a retrospective review of 254 children and young adults (age <1 month to 26 years) with pneumococcal pneumonia
(confirmed by blood or pleural fluid culture), the most common signs and symptoms and their approximate
frequencies are listed below [35]:
●Fever – 90 percent (mean duration three days before diagnosis)
●Cough – 70 percent; productive cough: 10 percent
●Tachypnea – 50 percent
●Malaise/lethargy – 45 percent
●Emesis – 43 percent
●Hypoxemia (oxygen saturation ≤95 percent) – 50 percent
●Decreased breath sounds – 55 percent
●Crackles – 40 percent
●Retractions – 30 percent
●Grunting – 25 percent
●Abdominal pain – 20 percent
●Chest pain – 10 percent
Radiographic features — Pneumococci can cause lobar or bronchopneumonia.
S. pneumoniae is the most common bacterial cause of sphere-shaped consolidation (ie, "round pneumonia").
However, this finding is not pathognomonic because round pneumonia can also be caused by other
streptococci, Haemophilus influenzae, staphylococci, Mycoplasma pneumoniae, lung abscess, and noninfectious
conditions. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Etiologic
clues'.)
Complications — In ambulatory children, pneumococcal pneumonia characteristically is uncomplicated, with
complete recovery of normal pulmonary architecture and function. However, complications occur in approximately 40
to 50 percent of children hospitalized with pneumococcal pneumonia [26,36]. Potential complications include [26,3639]:
●Pleural effusion
●Empyema
●Lung abscess
●Necrotizing pneumonia (particularly with serotype 3 and serogroup 19) (image 1)
●Atelectasis
●Pneumatocele
●Pneumothorax
In addition, pneumococcal pneumonia has been associated with hemolytic uremic syndrome [40,41]. (See"Overview
of hemolytic uremic syndrome in children", section on 'Streptococcus pneumoniae'.)
In a review of 111 children (0 to 16 years) hospitalized with confirmed pneumococcal pneumonia during 1986 to
1997, complicated pneumonia occurred in 39 percent [36]. More than one complication occurred in 60 percent of
patients; the distribution of complications was as follows:
●Pleural effusion – 83 percent
●Empyema – 52 percent
●Atelectasis – 26 percent
●Pneumatocele – 19 percent
●Pneumothorax – 10 percent
Complications correlated with weight ≤10th percentile for age, respiratory distress, anemia, and white blood cell
count <15,000/microL at the time of admission, but not with pneumococcal susceptibility to penicillin, chronic illness,
or comorbid conditions. Patients with complications had increased length of stay (13 versus 5 days) and duration of
fever (9 versus 2 days) compared with those without complications.
Advanced testing for viruses in children with bacterial pneumonia has revealed frequent coinfection. Although the
clinical significance of these viruses remains unclear, coinfection can be associated with a complicated course [4244].
Pneumococcal parapneumonic effusion/empyema is discussed briefly below and in greater detail separately.
(See "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and empyema in
children"and "Management and prognosis of parapneumonic effusion and empyema in children".) The other
complications are discussed separately. (See "Community-acquired pneumonia in children: Clinical features and
diagnosis", section on 'Complications'.)
Effusion/empyema — Data from the United States Pediatric Multicenter Pneumococcal Surveillance Group indicate
that the frequency of pneumococcal pneumonia complicated by loculated pleural effusion or empyema increased in
the period before the recommendation for universal immunization of infants with the pneumococcal conjugate vaccine
in 2000 [26]. Between 1993 and 2000, 368 children were hospitalized with culture-confirmed pneumococcal
pneumonia; 36 percent met criteria for pneumonia complicated by loculated pleural effusion or empyema.
(See "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and empyema in children",
section on 'Epidemiology' and "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and
empyema in children", section on 'Clinical presentation'.)
The incidence of pneumococcal parapneumonic empyema continued to increase after the recommendation for
routine immunization of infants in the United States with the pneumococcal conjugate vaccine [27,45,46]. In Utah's
Intermountain Healthcare system, pneumococcal parapneumonic effusion accounted for 17.5 percent of cases of
invasive pneumococcal disease in the period before routine vaccination (1996 to 2000) and 32 percent of cases of
invasive pneumococcal disease after routine vaccination. In both periods, serotype 1 was the most common cause of
pneumococcal parapneumonic empyema; in the period after routine vaccination, serogroups 3, 7F, and 19A also
were prevalent [27]. (See 'Serotypes' above.)
Parapneumonic effusions caused by strains intermediate or resistant to penicillin are associated with younger age
than those caused by susceptible organisms (two versus eight years). Parapneumonic effusions caused by strains
intermediate or resistant to penicillin usually are accompanied by bacteremia, but do not result in a poorer outcome
than susceptible strains [26,47,48].
The clinical features, diagnosis, and management of parapneumonic effusions are discussed separately.
(See"Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and empyema in children",
section on 'Clinical presentation' and "Management and prognosis of parapneumonic effusion and empyema in
children", section on 'Overview'.)
DIAGNOSIS — The history, physical findings, and finding of an infiltrate on chest radiograph usually establish the
diagnosis of pneumonia. Although lobar consolidation is suggestive of bacterial pneumonia, radiologists cannot
reliably differentiate bacterial from nonbacterial pneumonia on the basis of the radiographic appearance [49].
(See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Radiologic
evaluation'.)
Blood or pleural fluid cultures — Culture of the blood or pleural fluid is the most important method for identifying
the etiology of pneumonia. Among normal children hospitalized with pneumonia, approximately 10 to 15 percent have
positive cultures, primarily for S. pneumoniae. (See "Community-acquired pneumonia in children: Clinical features
and diagnosis", section on 'Cultures'.)
Antigen detection — Antigen detection by latex agglutination for pneumococcal polysaccharide in urine is not
sensitive enough to be useful. However, in children with parapneumonic effusion or empyema who were treated with
antibiotics before pleural fluid was obtained, detection of pneumococcal antigen in pleural fluid can confirm the
diagnosis [50]. (See "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and empyema in
children", section on 'Microbial analysis'.)
Polymerase chain reaction — Polymerase chain reaction (PCR) tests for pneumococcus in sputum and blood have
been developed [51,52]. However, the sensitivity and specificity of these tests in children have not been conclusively
established, and their routine use is not recommended [53,54].
Sputum Gram stain and culture — Among outpatients, pneumococcal pneumonia must be differentiated from other
causes of community-acquired pneumonia (CAP). However, an etiologic agent is identified in less than one-half of
cases [1]. Two problems make it difficult to identify the inciting organism: most children are unable to produce a
sputum specimen, and approximately 25 percent of patients have received antibiotics before presentation [35]. For
these and other reasons, sputum Gram stain and culture are of little value in children, and most patients with CAP are
treated empirically. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on
'Laboratory evaluation' and "Community-acquired pneumonia in children: Outpatient treatment", section on 'Empiric
therapy'.)
If a sputum sample is available, a Gram stain should be performed, and the specimen should be analyzed for the
presence of polymorphonuclear leukocytes (PMN), epithelial cells, and bacteria.
●A specimen that has more than 25 PMN and less than 10 epithelial cells per low power field (x100) represents
a purulent specimen. Individual microbiology laboratories may use slightly different criteria. However, all define
purulence based upon an increased number of PMN and a low (or absent) number of epithelial cells.
●The finding of a predominant organism (for example, gram-positive diplococci) may identify the cause of the
pneumonia (picture 1). When gram-positive, lancet-shaped diplococci are the predominant flora or there are
more than 10 gram-positive, lancet-shaped diplococci per oil immersion field (x1000), the sensitivity and
specificity for pneumococci identified by quellung reaction or culture are 62 percent and 85 percent,
respectively [55].
TREATMENT — The treatment recommendations below are consistent with those in the 2011 clinical practice
guidelines of the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America [56].
Supportive care — Supportive care for children with pneumonia is discussed separately. (See "Community-acquired
pneumonia in children: Outpatient treatment", section on 'Supportive care' and "Pneumonia in children: Inpatient
treatment", section on 'Supportive care'.)
Empiric therapy — Most patients with community-acquired pneumonia (CAP) are treated empirically. Whether or not
to include agents with activity against S. pneumoniae depends upon the age of the child, epidemiologic and clinical
information, and laboratory and imaging studies if such studies were obtained.
Empiric therapy for S. pneumoniae is generally included for children who require inpatient treatment for CAP and
children who have clinical findings compatible with bacterial pneumonia (eg, lobar or round consolidation on
radiograph, leukocytosis, elevated C-reactive protein, complications). Empiric therapy for CAP is discussed
separately. (See "Community-acquired pneumonia in children: Outpatient treatment", section on 'Empiric
therapy' and "Pneumonia in children: Inpatient treatment", section on 'Empiric therapy'.)
Children who are not critically ill can be treated with oral antibiotics. Some patients may benefit from initial parenteral
antibiotic therapy. In a retrospective study, children with bacteremic pneumococcal pneumonia who received initial
parenteral antibiotic followed by oral therapy were less likely to be admitted to the hospital (0 versus 24 percent) and
more likely to have their parents report improvement at follow-up (95 versus 67 percent) than were those who
received oral treatment alone [57].
Children who appear toxic or have evidence of complications, such as empyema, require intravenous therapy. For
children with serious allergic reactions to beta-lactam antibiotics, initial empiric therapy should
includevancomycin or clindamycin. (See "Pneumonia in children: Inpatient treatment", section on 'Empiric
therapy' and"Management and prognosis of parapneumonic effusion and empyema in children", section on 'Antibiotic
therapy'.)
Specific therapy — When there is a positive culture for S. pneumoniae, the antibiotic susceptibility pattern (table 3)
should guide therapy. Parenteral and oral regimens for anti-pneumococcal agents are provided in the table (table 4).
Penicillin-susceptible strains — Penicillin or ampicillin is the drug of choice for parenteral treatment of
pneumococcal pneumonia caused by isolates with penicillin MICs ≤2 mcg/mL (table 3 and table 4) [56,58-63].
Penicillin and ampicillin are less expensive than alternative agents for penicillin-susceptible strains. Alternative
parenteral therapies (if the isolate is susceptible) include cefotaxime, ceftriaxone, clindamycin, vancomycin,
andlevofloxacin if the isolate is susceptible. Clindamycin is an alternative for patients with severe hypersensitivity to
beta-lactam antibiotics. Ceftriaxone is preferred for outpatient parenteral therapy. Vancomycin may be warranted for
children with severe hypersensitivity to beta-lactam antibiotics and an isolate resistant to clindamycin.
Oral amoxicillin is the drug of choice for oral treatment of pneumococcal pneumonia caused by isolates with penicillin
MICs ≤2 mcg/mL. Alternative oral therapies (if the isolate is susceptible) include cefpodoxime,cefprozil, cefuroxime,
and levofloxacin (table 4). Clindamycin is an alternative for patients with severe hypersensitivity to beta-lactam
antibiotics if the isolate is susceptible (table 3).
Intermediate and resistant strains — Ceftriaxone or cefotaxime are preferred for parenteral treatment for
pneumococcal pneumonia caused by isolates with penicillin MICs >2 mcg/mL (table 3 and table
4). Vancomycin,levofloxacin, linezolid, and clindamycin are alternatives. Nonsusceptibility to ceftriaxone or
cefotaxime appears to be decreasing with the decreasing frequency of serotype 19A (which is included in the 13valent pneumococcal conjugate vaccine, licensed in 2010) [64,65].
Oral levofloxacin or linezolid are the drugs of choice for oral treatment of pneumococcal pneumonia caused by
isolates with penicillin MICs >2 mcg/mL. Clindamycin is an alternative parenteral or oral therapy (if the isolate is
susceptible).
Clones of the pneumococcal serotype 19A in particular may be resistant to penicillin, macrolides, clindamycin,
and trimethoprim-sulfamethoxazole. Such multidrug-resistant isolates may require treatment
with vancomycin,linezolid, or levofloxacin [66-68].
Duration of therapy — Therapy generally is continued for a total period of five to seven days for uncomplicated
pneumonia or until the patient is afebrile for five days in more severe cases. (See "Community-acquired pneumonia in
children: Outpatient treatment", section on 'Duration' and "Pneumonia in children: Inpatient treatment", section on
'Duration of treatment'.)
Empyema — The treatment of empyema is discussed separately. (See "Management and prognosis of
parapneumonic effusion and empyema in children".)
RESPONSE TO THERAPY — Children with pneumonia who are appropriately treated should show signs of
improvement within 24 to 48 hours. Failure to improve as anticipated may indicate:
●Alternative or coincident diagnosis (eg, foreign body aspiration) (see "Community-acquired pneumonia in
children: Clinical features and diagnosis", section on 'Differential diagnosis')
●Ineffective antibiotic coverage (eg, resistant organism) (see "Resistance of Streptococcus pneumoniae to
beta-lactam antibiotics" and "Resistance of Streptococcus pneumoniae to the macrolides, azalides,
lincosamines, and ketolides" and "Resistance of Streptococcus pneumoniae to the fluoroquinolones,
doxycycline, and trimethoprim-sulfamethoxazole")
●Development of complications (see 'Complications' above)
These possibilities are discussed separately. (See "Community-acquired pneumonia in children: Outpatient
treatment", section on 'Treatment failure' and "Pneumonia in children: Inpatient treatment", section on 'Treatment
failure'.)
FOLLOW-UP — The clinical and radiographic follow-up for children with pneumonia are discussed separately.
(See "Pneumonia in children: Inpatient treatment", section on 'Follow-up' and "Community-acquired pneumonia in
children: Outpatient treatment", section on 'Follow-up'.)
OUTCOME — Most otherwise healthy children with pneumococcal pneumonia, even complicated pneumococcal
pneumonia, recover without sequelae. The Centers for Disease Control and Prevention (CDC) examined
pneumococcal pneumonia in 5837 patients from nine geographic areas in the United States; 7 percent were younger
than 18 years old [69]. The case fatality rates for pneumococcal pneumonia for children in the United States from
1995 to 1997 (not adjusted for comorbid conditions) were estimated to be 4 percent in children younger than two
years and 2 percent in children 2 to 17 years [69].
PREVENTION
Infection control — Standard isolation precautions are recommended for children with pneumococcal pneumonia
[2]. (See "General principles of infection control", section on 'Standard precautions'.)
Active immunization — Immunization with the pneumococcal conjugate vaccine (PCV) is recommended for all
infants in the United States. The efficacy of PCV in preventing pneumonia is discussed separately.
(See"Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children", section on 'Indications'.)
Children who are at increased risk of invasive pneumococcal disease (table 2) also should receive thepneumococcal
polysaccharide vaccine beginning at two years of age; the pneumococcal polysaccharide vaccine should be
administered at least eight weeks after PCV. (See "Pneumococcal (Streptococcus pneumoniae) polysaccharide
vaccines in children", section on 'Indications'.)
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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 education: Pneumonia in children (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Streptococcus pneumoniae is the most common cause of bacterial pneumonia. However, in certain age
groups, other causes of pneumonia predominate. (See 'Burden of disease' above and "Pneumonia in children:
Epidemiology, pathogenesis, and etiology", section on 'Etiologic agents'.)
●The most common clinical manifestations of pneumococcal pneumonia are fever, non-productive cough,
tachypnea, and decreased breath sounds over the affected area. Auscultatory findings of crepitant rales
(crackles) and tubular breath sounds are highly localized to the involved segment or lobe. (See 'Clinical
manifestations' above.)
●Complications, which are present in 40 to 50 percent of children hospitalized with pneumococcal pneumonia,
include pleural effusion, empyema, lung abscess, necrotizing pneumonia, atelectasis, pneumatocele, and
pneumothorax. (See 'Complications' above.)
●History, examination, and radiographic findings usually establish the diagnosis of pneumonia. Although lobar
consolidation is suggestive of bacterial pneumonia, radiographic features cannot reliably differentiate bacterial
from nonbacterial pneumonia. Specific diagnosis of pneumococcal pneumonia in children is usually made
through culture of the blood or pleural fluid. (See 'Diagnosis' above.)
●Most patients with community-acquired pneumonia are treated empirically. If S. pneumoniae is a
consideration, empiric therapy generally includes a beta-lactam antibiotic (ie, penicillin or cephalosporin).
Children who appear toxic or have evidence of complications require intravenous therapy. Children who are not
critically ill can be treated orally. (See 'Empiric therapy' above.)
●When there is a positive culture for S. pneumoniae, the antibiotic susceptibility pattern should guide therapy
(table 3). (See 'Specific therapy' above.)
•We suggest penicillin or ampicillin as the parenteral drug of choice and amoxicillin as the oral drug of
choice for pneumococcal pneumonia caused by isolates with penicillin MICs ≤2 mcg/mL (Grade 2B).
Alternative parenteral agents include cefotaxime, ceftriaxone, clindamycin, vancomycin, or levofloxacinif
the isolate is susceptible. Alternative oral therapies include cefpodoxime, cefprozil, cefuroxime,
levofloxacin. Doses are provided in the table (table 4).
•We suggest ceftriaxone or cefotaxime as the preferred parenteral treatment and
oral levofloxacin orlinezolid as the preferred oral treatment for pneumococcal isolates with penicillin MICs
>2 mcg/mL(table 4) (Grade 2C). Vancomycin, levofloxacin, linezolid, and clindamycin (if the isolate is
susceptible) are alternatives.
●Therapy generally is continued for five to seven days for uncomplicated disease or until the patient is afebrile
for five days in more severe cases. (See 'Duration of therapy' above.)
●Most otherwise-healthy children with pneumococcal pneumonia, even complicated pneumococcal pneumonia,
recover without sequelae. The case fatality rates for pneumococcal pneumonia for children in the United States
are estimated to be 4 percent in children younger than two years and 2 percent in children 2 to 17 years.
(See 'Outcome' above.)
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