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Pneumococcal pneumonia in children

Pneumococcal pneumonia in children
Literature review current through: Jan 2024.
This topic last updated: Feb 28, 2023.

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 is a significant problem worldwide. 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 "Streptococcus pneumoniae: Microbiology and pathogenesis of infection".)

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 (PCV) [7-10]. Higher pneumococcal carriage rates (up to 90 percent) have been described in resource-limited countries with low vaccination coverage [11]. Pneumococcal acquisition is also common in adults, particularly those who live with children. In a small study, approximately 20 percent of adults were intermittent carriers and 10 percent were carriers for >4 months (median duration seven weeks) [12]. (See "Streptococcus pneumoniae: Microbiology and pathogenesis of infection", section on 'Pathogenesis'.)

Antibiotic-resistant strains remain a concern but penicillin resistance has declined since the introduction of PCVs [11,13-15]. (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, and lincosamides".)

Invasive disease most commonly occurs upon acquisition of a new serotype, typically after an incubation period of one to three days.

Pneumococci are presumably aerosolized from the nasopharynx to the alveolus, where they interact with alveolar type II cells and activate innate and cellular host defenses. Given the strong association of pneumococcal disease with viral illness [16-21], it is believed that viral activation of respiratory epithelial cells may increase expression of receptors for pneumococcal attachment and decrease the capacity of the pulmonary immune response to clear bacteria [22].

The pneumonic lesion progresses as pneumococci multiply in the alveolus and invade the alveolar epithelium. Pneumococci pass from alveolus to alveolus creating inflammation and consolidation strictly along lobar compartments. The center of the spreading lesion shows more advanced inflammation than do the edges. Lung consolidation evolves over two to three days and remains prominent after fever resolves [23-25].

EPIDEMIOLOGY

Burden of disease — Pneumonia is a common cause of death in children worldwide [26]. Community-acquired pneumonia (CAP) can be caused by a variety of bacterial and viral pathogens, and the predominant pathogen varies with age. S. pneumoniae is the most common typical bacterial cause of CAP, although in many cases an organism cannot be isolated. (See "Pneumonia in children: Epidemiology, pathogenesis, and etiology", section on 'Community-acquired pneumonia'.)

In the United States, the incidence of pneumococcal pneumonia in children declined after the 7-valent pneumococcal conjugate vaccine (PCV7) was replaced with the 13-valent pneumococcal conjugate vaccine (PCV13) in 2010 [27-29]. A 2023 systematic review including studies from most World Health Organization regions reported a median decline of 69 percent in hospitalization rates due to bacteremic pneumococcal pneumonia in children <5 years of age after introduction of PCV13 or the 10-valent pneumococcal conjugate vaccine (PCV10) [30]. However, vaccine-induced protection from pneumonia remains modest at best, in contrast to potent efficacy against bacteremia. (See "Pneumococcal vaccination in children", section on 'Pneumonia and empyema'.)

Serotypes — The pneumococcal serotypes isolated from children with pneumococcal pneumonia have changed with the introduction of PCVs (table 1) to the routine childhood immunization schedule in the United States. 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 [31-36]. PCV13, which contains all of these serotypes except 12, replaced PCV7 in 2010. However, between 2014 and 2017, 50 of 119 (42 percent) isolates from children hospitalized with culture-proven pneumococcal pneumonia at the eight children's hospitals in the United States Pediatric Multicenter Pneumococcal Surveillance Study Group were PCV13 serotypes; 19A and 3 were most common [28,37]. Serotype 3 remains an important cause of complicated pneumonia in children despite widespread use of PCV13 [38,39]. A 15-valent pneumococcal conjugate vaccine (PCV15) that contains serotypes 22F and 33F in addition to those in PCV13 was licensed for use in children in the United States in 2022 and can be used interchangeably with PCV13. (See 'Complications' below and "Pneumococcal vaccination in children", section on 'Conjugate vaccines'.)

Risk factors — Risk factors for invasive pneumococcal disease are listed in the table (table 2).

Antibiotic resistance — Resistance of S. pneumoniae to multiple antibiotics was an increasingly important clinical problem before the introduction of PCVs. Resistance continues to develop in strains that emerge in nonvaccine serotypes. 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, and lincosamides" 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 day [2].

Clinical manifestations — Pneumococcal pneumonia is the paradigm of classic lobar bacterial pneumonia [23]. 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 [40]:

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, Staphylococcus aureus, 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 70 percent of children hospitalized with pneumococcal pneumonia [28,41,42].

In reviews of children hospitalized with confirmed pneumococcal pneumonia, the frequencies of pulmonary complications (which were not mutually exclusive) were as follows [28,41,42]:

Pleural effusion – 36 to 83 percent

Empyema – 49 to 52 percent

Necrotizing pneumonia – 31 percent

Lung abscess (image 1) – 5 percent

Pneumatocele – 19 percent

Pneumothorax – 10 percent

In addition, cardiac events are common during acute pneumococcal pneumonia and recovery from acute pneumococcal pneumonia [43,44]. These events are readily recognizable in adults and may also occur in children. In a nonhuman primate model, pneumococcal microlesions arose in the myocardium during pneumonia and led to arrhythmias and acute coronary syndromes [45].

Pneumococcal pneumonia has also been associated with hemolytic uremic syndrome [46,47]. In a review from the post-PCV era, 4 percent of children hospitalized with pneumococcal pneumonia had hemolytic uremic syndrome [28]. (See "Overview of hemolytic uremic syndrome in children", section on 'Streptococcus pneumoniae'.)

In the post-PCV era, complicated pneumonia was associated with longer duration of fever before admission (5 versus 2 days), longer hospitalization (12 versus 5 days), and longer duration of antibiotic therapy (21 versus 14 days) [28]. Comorbidity (eg, sickle cell disease) was more common in children with uncomplicated than complicated pneumonia (52 versus 23 percent). The rate of viral co-infection was similar in children with complicated and uncomplicated pneumonia (approximately 25 percent).

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" and "Management and prognosis of parapneumonic effusion and empyema in children".)

The clinical features and diagnosis of the other complications are discussed separately. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Complications'.)

DIAGNOSIS

Community-acquired pneumonia — 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 [48]. The approach to diagnosis of community-acquired pneumonia (CAP) in children is discussed separately. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Diagnosis'.)

Pneumococcal pneumonia — Confirmation of pneumococcal pneumonia is necessary to provide targeted antimicrobial therapy. This is particularly important in children who are admitted to the hospital. Etiologic testing is not usually recommended for children who will be treated as outpatients. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Etiologic diagnosis'.)

The following sections describe the utility of various microbiologic tests for identifying S. pneumoniae as the etiology in children with a clinical diagnosis of pneumonia. However, standard diagnostic testing (blood culture, sputum culture, and pneumococcal urinary antigen test [for adults]) detects S. pneumoniae in <30 percent of cases of CAP [49].

Blood cultures – Cultures of the blood are an important method for identifying the etiology of pneumonia. In a cross-sectional study of previously healthy children hospitalized with CAP (according to discharge diagnosis code), 2.5 percent of blood cultures were positive; among the positive cultures, 78 percent grew S. pneumoniae [50]. Higher rates of positive blood cultures are likely in children with radiographically confirmed CAP or complicated pneumonia [51]. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Approach to microbiologic testing'.)

Pleural fluid cultures – Pleural fluid cultures are an important method for identifying the etiology of pneumonia. The indications for obtaining and testing pleural fluid are discussed separately. (See "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children", section on 'Evaluation'.)

Sputum Gram stain and culture – Sputum Gram stain and culture are of little value in children because most children are unable to produce an adequate sputum specimen and many have received antibiotics before presentation.

If the child is able to produce an adequate sputum sample, 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 predominant gram-positive diplococci (picture 1) may suggest S. pneumoniae as the cause of pneumonia. However, in a prospective study, sputum culture detected <10 percent of cases of pneumococcal CAP [52].

Polymerase chain reaction – Polymerase chain reaction (PCR) tests for pneumococcus in sputum and blood have been developed [53,54]. Improved sensitivity (57 percent) and specificity (85 percent) of diagnosis has been achieved by targeting the autolysin lytA gene for quantitative PCR [55]. This improvement suggests PCR as a diagnostic method of choice in children. In a prospective study, PCR detected approximately 25 percent of cases of pneumococcal pneumonia, while sputum culture detected <10 percent [52].

Pleural fluid PCR can detect evidence of S. pneumoniae in patients with culture-negative pleural fluid and is increasingly available, particularly in large children's hospitals [56]. In a prospective study of children with parapneumonic effusion and pleural empyema, 45 percent of pleural fluid samples were PCR positive for a respiratory pathogen; of those, 90 percent were S. pneumoniae positive [57].

Antigen detection – Although the urine antigen test for S. pneumoniae is sensitive in adult patients (ranging from 59 to 87 percent) [49], it is not recommended for diagnosing pneumococcal pneumonia in children because it may be positive in children with asymptomatic colonization as well in children with pneumococcal disease [58-60]. On the other hand, given its high specificity (>90 percent) [49], a negative urine antigen test is helpful in excluding S. pneumoniae.

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 [61]. (See "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children", section on 'Microbial analysis'.)

TREATMENT — The treatment recommendations below are consistent with those in the clinical practice guidelines of the American Academy of Pediatrics [2] and the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America [59].

Supportive care — Supportive care for children with pneumonia is discussed separately. (See "Pneumonia in children: Inpatient treatment", section on 'Supportive care' and "Community-acquired pneumonia in children: Outpatient 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 "Pneumonia in children: Inpatient treatment", section on 'Empiric therapy' and "Community-acquired pneumonia in children: Outpatient treatment", section on 'Empiric therapy'.)

Specific therapy

Positive culture — When there is a positive culture for S. pneumoniae, the antibiotic susceptibility pattern (table 3) should guide therapy. Parenteral and oral regimens for antipneumococcal 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) [59,62-67]. Penicillin and ampicillin are less expensive and have a narrower spectrum of activity than alternative agents for penicillin-susceptible strains. Alternative parenteral therapies (if the isolate is susceptible) include ceftriaxone (or cefotaxime if available), clindamycin, vancomycin, and levofloxacin. 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, an isolate resistant to clindamycin, or life-threatening infection.

Oral amoxicillin is the drug of choice for oral treatment of pneumococcal pneumonia caused by isolates with penicillin MICs ≤2 mcg/mL. It is less expensive and has a narrower spectrum of activity than alternative agents. Alternative oral therapies (if the isolate is susceptible) include cefpodoxime, cefprozil, cefuroxime, and levofloxacin (table 4). Cefpodoxime, cefprozil, and cefuroxime are the only oral cephalosporins recommended for the treatment of pneumococcal pneumonia. Clindamycin or levofloxacin are alternatives for patients with severe hypersensitivity to beta-lactam antibiotics if the isolate is susceptible (table 3).

Penicillin-intermediate and resistant strainsCeftriaxone or cefotaxime are preferred for parenteral treatment for pneumococcal pneumonia caused by isolates with penicillin MICs ≥4 mcg/mL (table 3 and table 4). Nonsusceptibility to ceftriaxone or cefotaxime appears to be decreasing with the decreasing frequency of serotype 19A (which is included in the 13-valent (PCV13) and 15-valent pneumococcal conjugate vaccines, licensed in 2010 and 2022, respectively) [68,69]. Ceftaroline, vancomycin, levofloxacin, linezolid, and clindamycin are alternatives to ceftriaxone or cefotaxime.

Oral levofloxacin or linezolid are the drugs of choice for oral treatment of pneumococcal pneumonia caused by isolates with penicillin MICs ≥4 mcg/mL. Clindamycin is an alternative parenteral or oral therapy (if the isolate is susceptible).

Before licensure of PCV13, clones of the pneumococcal serotype 19A often were resistant to penicillin, macrolides, clindamycin, and trimethoprim-sulfamethoxazole [70-72]. In the post-PCV13 era, serotypes 35B and 15A have the highest incidence of multidrug nonsusceptibility among isolates causing invasive pneumococcal disease [15]. Such multidrug-resistant isolates may require treatment with vancomycin, linezolid, ceftaroline, or levofloxacin.

Negative culture — For children whose cultures are negative for S. pneumoniae (eg, because of pretreatment with antibiotics), but who are presumed to have S. pneumoniae, we continue initial empiric therapy, provided that the child has responded as expected to the first 24 to 48 hours of treatment. For children who fail to improve or who worsen during initial empiric therapy, after excluding a complication that requires source control, we change antibiotics to include activity against penicillin-intermediate or penicillin-resistant S. pneumoniae as described above.

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, and lincosamides" 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.

Before the introduction of pneumococcal conjugate vaccines, case fatality rates for pneumococcal pneumonia for children in the United States were estimated to be 4 percent in children younger than two years and 2 percent in children 2 to 17 years [73].

The introduction of pneumococcal conjugate vaccines has resulted in a dramatic reduction in invasive disease and mortality rates in the countries in which they have been introduced [74]. However, pneumococcal pneumonia mortality rates have not been specifically examined. Data from the United States Pediatric Multicenter Pneumococcal Surveillance Study Group demonstrated overall pneumococcal mortality rates of 1 percent after the introduction of PCV7 (during 2006 to 2009) and 0 percent after the introduction of PCV13 (during 2011 to 2014) [75].

In a study from eastern Gambia, introduction of a nine-valent pneumococcal conjugate vaccine resulted in reduced all-cause mortality (25 versus 30 deaths per 1000 child-years) [76].

Additional details regarding morbidity and mortality from invasive pneumococcal disease before and after the era of routine pneumococcal vaccination are provided separately. (See "Pneumococcal vaccination in children", section on 'Efficacy and effectiveness'.)

PREVENTION

Infection control — Standard isolation precautions are recommended for children with pneumococcal pneumonia [2]. (See "Infection prevention: Precautions for preventing transmission of infection", 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 vaccination in children", section on 'Immunization of high-risk children and adolescents'.)

Children who are at increased risk of invasive pneumococcal disease (table 2) also should receive the pneumococcal polysaccharide vaccine (PPSV) beginning at two years of age; PPSV should be administered at least eight weeks after PCV.

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

SUMMARY AND RECOMMENDATIONS

Epidemiology – Streptococcus pneumoniae is the most common cause of typical 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'.)

Clinical manifestations – The most common clinical manifestations of pneumococcal pneumonia 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. (See 'Clinical manifestations' above.)

Complications – Complications, which are present in 40 to 70 percent of children hospitalized with pneumococcal pneumonia, include pleural effusion, empyema, lung abscess, necrotizing pneumonia, pneumatocele, and pneumothorax. (See 'Complications' above.)

Evaluation and diagnosis – 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.)

Management

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). (See 'Empiric therapy' above and "Pneumonia in children: Inpatient treatment", section on 'Empiric therapy' and "Community-acquired pneumonia in children: Outpatient treatment", section on 'Summary and recommendations'.)

When there is a positive culture for S. pneumoniae, the antibiotic susceptibility pattern should guide therapy (table 3 and table 4). (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 minimum inhibitory concentrations (MICs) ≤2 mcg/mL (Grade 2C). Alternative parenteral agents include cefotaxime, ceftriaxone, ceftaroline, clindamycin, vancomycin, or levofloxacin if the isolate is susceptible. Alternative oral therapies include cefpodoxime, cefprozil, cefuroxime, or levofloxacin. Doses are provided in the table (table 4).

-We suggest ceftriaxone or cefotaxime as the preferred parenteral treatment and oral levofloxacin or linezolid as the preferred oral treatment for pneumococcal isolates with penicillin MICs ≥4 mcg/mL (table 4) (Grade 2C). Ceftaroline, 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.)

Outcome – 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.)

  1. Wubbel L, Muniz L, Ahmed A, et al. Etiology and treatment of community-acquired pneumonia in ambulatory children. Pediatr Infect Dis J 1999; 18:98.
  2. American Academy of Pediatrics. Streptococcus pneumoniae (pneumococcal) infections. In: Red Book: 2021-2024 Report of the Committee on Infectious Diseases, 32nd ed, Kimberlin DW, Barnett ED, Lynfield R, Sawyer MH (Eds), American Academy of Pediatrics, Itasca, IL 2021. p.717.
  3. Thornsberry C, Ogilvie PT, Holley HP Jr, Sahm DF. Survey of susceptibilities of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis isolates to 26 antimicrobial agents: a prospective U.S. study. Antimicrob Agents Chemother 1999; 43:2612.
  4. Sisson BA, Buck G, Franco SM, et al. Penicillin minimum inhibitory concentration drift in identical sequential Streptococcus pneumoniae isolates from colonized healthy infants. Clin Infect Dis 2000; 30:191.
  5. Raymond J, Le Thomas I, Moulin F, et al. Sequential colonization by Streptococcus pneumoniae of healthy children living in an orphanage. J Infect Dis 2000; 181:1983.
  6. Austrian R. Some aspects of the pneumococcal carrier state. J Antimicrob Chemother 1986; 18 Suppl A:35.
  7. Millar EV, O'Brien KL, Watt JP, et al. Effect of community-wide conjugate pneumococcal vaccine use in infancy on nasopharyngeal carriage through 3 years of age: a cross-sectional study in a high-risk population. Clin Infect Dis 2006; 43:8.
  8. Huang SS, Platt R, Rifas-Shiman SL, et al. Post-PCV7 changes in colonizing pneumococcal serotypes in 16 Massachusetts communities, 2001 and 2004. Pediatrics 2005; 116:e408.
  9. Park SY, Moore MR, Bruden DL, et al. Impact of conjugate vaccine on transmission of antimicrobial-resistant Streptococcus pneumoniae among Alaskan children. Pediatr Infect Dis J 2008; 27:335.
  10. Dananché C, Paranhos-Baccalà G, Messaoudi M, et al. Serotypes of Streptococcus pneumoniae in Children Aged <5 Years Hospitalized With or Without Pneumonia in Developing and Emerging Countries: A Descriptive, Multicenter Study. Clin Infect Dis 2020; 70:875.
  11. Tvedskov ESF, Hovmand N, Benfield T, Tinggaard M. Pneumococcal carriage among children in low and lower-middle-income countries: A systematic review. Int J Infect Dis 2022; 115:1.
  12. Almeida ST, Paulo AC, Froes F, et al. Dynamics of Pneumococcal Carriage in Adults: A New Look at an Old Paradigm. J Infect Dis 2021; 223:1590.
  13. Ben-Shimol S, Givon-Lavi N, Greenberg D, et al. Impact of pneumococcal conjugate vaccines introduction on antibiotic resistance of Streptococcus pneumoniae meningitis in children aged 5 years or younger, Israel, 2004 to 2016. Euro Surveill 2018; 23.
  14. Pilishvili T, Lexau C, Farley MM, et al. Sustained reductions in invasive pneumococcal disease in the era of conjugate vaccine. J Infect Dis 2010; 201:32.
  15. Bajema KL, Gierke R, Farley MM, et al. Impact of Pneumococcal Conjugate Vaccines on Antibiotic-Nonsusceptible Invasive Pneumococcal Disease in the United States. J Infect Dis 2022; 226:342.
  16. Madhi SA, Klugman KP, Vaccine Trialist Group. A role for Streptococcus pneumoniae in virus-associated pneumonia. Nat Med 2004; 10:811.
  17. Madhi SA, Ludewick H, Kuwanda L, et al. Pneumococcal coinfection with human metapneumovirus. J Infect Dis 2006; 193:1236.
  18. Ampofo K, Bender J, Sheng X, et al. Seasonal invasive pneumococcal disease in children: role of preceding respiratory viral infection. Pediatrics 2008; 122:229.
  19. O'Brien KL, Walters MI, Sellman J, et al. Severe pneumococcal pneumonia in previously healthy children: the role of preceding influenza infection. Clin Infect Dis 2000; 30:784.
  20. Danino D, Ben-Shimol S, van der Beek BA, et al. Decline in Pneumococcal Disease in Young Children During the Coronavirus Disease 2019 (COVID-19) Pandemic in Israel Associated With Suppression of Seasonal Respiratory Viruses, Despite Persistent Pneumococcal Carriage: A Prospective Cohort Study. Clin Infect Dis 2022; 75:e1154.
  21. Sarmiento Clemente A, Kaplan SL, Barson WJ, et al. Decrease in Pediatric Invasive Pneumococcal Disease During the COVID-19 Pandemic. J Pediatric Infect Dis Soc 2022; 11:426.
  22. Tuomanen EI, Austrian R, Masure HR. Pathogenesis of pneumococcal infection. N Engl J Med 1995; 332:1280.
  23. Heffron R. Pneumonia. Commonwealth Fund, New York 1939.
  24. Tuomanen E, Rich R, Zak O. Induction of pulmonary inflammation by components of the pneumococcal cell surface. Am Rev Respir Dis 1987; 135:869.
  25. Bergeron Y, Ouellet N, Deslauriers AM, et al. Cytokine kinetics and other host factors in response to pneumococcal pulmonary infection in mice. Infect Immun 1998; 66:912.
  26. Global Burden of Disease Child and Adolescent Health Collaboration, Kassebaum N, Kyu HH, et al. Child and Adolescent Health From 1990 to 2015: Findings From the Global Burden of Diseases, Injuries, and Risk Factors 2015 Study. JAMA Pediatr 2017; 171:573.
  27. Moore MR, Link-Gelles R, Schaffner W, et al. Effect of use of 13-valent pneumococcal conjugate vaccine in children on invasive pneumococcal disease in children and adults in the USA: analysis of multisite, population-based surveillance. Lancet Infect Dis 2015; 15:301.
  28. Olarte L, Barson WJ, Barson RM, et al. Pneumococcal Pneumonia Requiring Hospitalization in US Children in the 13-Valent Pneumococcal Conjugate Vaccine Era. Clin Infect Dis 2017; 64:1699.
  29. Ouldali N, Levy C, Minodier P, et al. Long-term Association of 13-Valent Pneumococcal Conjugate Vaccine Implementation With Rates of Community-Acquired Pneumonia in Children. JAMA Pediatr 2019; 173:362.
  30. Reyburn R, Tsatsaronis A, von Mollendorf C, et al. Systematic review on the impact of the pneumococcal conjugate vaccine ten valent (PCV10) or thirteen valent (PCV13) on all-cause, radiologically confirmed and severe pneumonia hospitalisation rates and pneumonia mortality in children 0-9 years old. J Glob Health 2023; 13:05002.
  31. Byington CL, Hulten KG, Ampofo K, et al. Molecular epidemiology of pediatric pneumococcal empyema from 2001 to 2007 in Utah. J Clin Microbiol 2010; 48:520.
  32. Schutze GE, Tucker NC, Mason EO Jr. Impact of the conjugate pneumococcal vaccine in arkansas. Pediatr Infect Dis J 2004; 23:1125.
  33. Byington CL, Samore MH, Stoddard GJ, et al. Temporal trends of invasive disease due to Streptococcus pneumoniae among children in the intermountain west: emergence of nonvaccine serogroups. Clin Infect Dis 2005; 41:21.
  34. Chibuk TK, Robinson JL, Hartfield DS. Pediatric complicated pneumonia and pneumococcal serotype replacement: trends in hospitalized children pre and post introduction of routine vaccination with Pneumococcal Conjugate Vaccine (PCV7). Eur J Pediatr 2010; 169:1123.
  35. Yu J, Salamon D, Marcon M, Nahm MH. Pneumococcal serotypes causing pneumonia with pleural effusion in pediatric patients. J Clin Microbiol 2011; 49:534.
  36. Thomas MF, Sheppard CL, Guiver M, et al. Emergence of pneumococcal 19A empyema in UK children. Arch Dis Child 2012; 97:1070.
  37. Kaplan SL, Barson WJ, Lin PL, et al. Invasive Pneumococcal Disease in Children's Hospitals: 2014-2017. Pediatrics 2019; 144.
  38. Silva-Costa C, Gomes-Silva J, Pinho MD, et al. Continued Vaccine Breakthrough Cases of Serotype 3 Complicated Pneumonia in Vaccinated Children, Portugal (2016-2019). Microbiol Spectr 2022; 10:e0107722.
  39. Lapidot R, Shea KM, Yildirim I, et al. Characteristics of Serotype 3 Invasive Pneumococcal Disease before and after Universal Childhood Immunization with PCV13 in Massachusetts. Pathogens 2020; 9.
  40. Tan TQ, Mason EO Jr, Barson WJ, et al. Clinical characteristics and outcome of children with pneumonia attributable to penicillin-susceptible and penicillin-nonsusceptible Streptococcus pneumoniae. Pediatrics 1998; 102:1369.
  41. Tan TQ, Mason EO Jr, Wald ER, et al. Clinical characteristics of children with complicated pneumonia caused by Streptococcus pneumoniae. Pediatrics 2002; 110:1.
  42. Wexler ID, Knoll S, Picard E, et al. Clinical characteristics and outcome of complicated pneumococcal pneumonia in a pediatric population. Pediatr Pulmonol 2006; 41:726.
  43. Sandvall B, Rueda AM, Musher DM. Long-term survival following pneumococcal pneumonia. Clin Infect Dis 2013; 56:1145.
  44. Violi F, Cangemi R, Falcone M, et al. Cardiovascular Complications and Short-term Mortality Risk in Community-Acquired Pneumonia. Clin Infect Dis 2017; 64:1486.
  45. Reyes LF, Restrepo MI, Hinojosa CA, et al. Severe Pneumococcal Pneumonia Causes Acute Cardiac Toxicity and Subsequent Cardiac Remodeling. Am J Respir Crit Care Med 2017; 196:609.
  46. Waters AM, Kerecuk L, Luk D, et al. Hemolytic uremic syndrome associated with invasive pneumococcal disease: the United kingdom experience. J Pediatr 2007; 151:140.
  47. Bender JM, Ampofo K, Byington CL, et al. Epidemiology of Streptococcus pneumoniae-induced hemolytic uremic syndrome in Utah children. Pediatr Infect Dis J 2010; 29:712.
  48. Marrie TJ. Community-acquired pneumonia. Clin Infect Dis 1994; 18:501.
  49. Laijen W, Snijders D, Boersma WG. Pneumococcal urinary antigen test: diagnostic yield and impact on antibiotic treatment. Clin Respir J 2017; 11:999.
  50. Neuman MI, Hall M, Lipsett SC, et al. Utility of Blood Culture Among Children Hospitalized With Community-Acquired Pneumonia. Pediatrics 2017; 140.
  51. Myers AL, Hall M, Williams DJ, et al. Prevalence of bacteremia in hospitalized pediatric patients with community-acquired pneumonia. Pediatr Infect Dis J 2013; 32:736.
  52. Cvitkovic Spik V, Beovic B, Pokorn M, et al. Improvement of pneumococcal pneumonia diagnostics by the use of rt-PCR on plasma and respiratory samples. Scand J Infect Dis 2013; 45:731.
  53. Resti M, Moriondo M, Cortimiglia M, et al. Community‐acquired bacteremic pneumococcal pneumonia in children: diagnosis and serotyping by real‐time polymerase chain reaction using blood samples. Clin Infect Dis 2010; 51:1042.
  54. Azzari C, Moriondo M, Indolfi G, et al. Realtime PCR is more sensitive than multiplex PCR for diagnosis and serotyping in children with culture negative pneumococcal invasive disease. PLoS One 2010; 5:e9282.
  55. van Schaik ML, Duijkers R, Paternotte N, et al. Feasibility of a quantitative polymerase chain reaction assay for diagnosing pneumococcal pneumonia using oropharyngeal swabs. Mol Biol Rep 2019; 46:1013.
  56. Blaschke AJ, Heyrend C, Byington CL, et al. Molecular analysis improves pathogen identification and epidemiologic study of pediatric parapneumonic empyema. Pediatr Infect Dis J 2011; 30:289.
  57. Krenke K, Sadowy E, Podsiadły E, et al. Etiology of parapneumonic effusion and pleural empyema in children. The role of conventional and molecular microbiological tests. Respir Med 2016; 116:28.
  58. Klugman KP, Madhi SA, Albrich WC. Novel approaches to the identification of Streptococcus pneumoniae as the cause of community-acquired pneumonia. Clin Infect Dis 2008; 47 Suppl 3:S202.
  59. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis 2011; 53:e25.
  60. Dowell SF, Garman RL, Liu G, et al. Evaluation of Binax NOW, an assay for the detection of pneumococcal antigen in urine samples, performed among pediatric patients. Clin Infect Dis 2001; 32:824.
  61. Le Monnier A, Carbonnelle E, Zahar JR, et al. Microbiological diagnosis of empyema in children: comparative evaluations by culture, polymerase chain reaction, and pneumococcal antigen detection in pleural fluids. Clin Infect Dis 2006; 42:1135.
  62. Choi EH, Lee HJ. Clinical outcome of invasive infections by penicillin-resistant Streptococcus pneumoniae in Korean children. Clin Infect Dis 1998; 26:1346.
  63. Deeks SL, Palacio R, Ruvinsky R, et al. Risk factors and course of illness among children with invasive penicillin-resistant Streptococcus pneumoniae. The Streptococcus pneumoniae Working Group. Pediatrics 1999; 103:409.
  64. Cardoso MR, Nascimento-Carvalho CM, Ferrero F, et al. Penicillin-resistant pneumococcus and risk of treatment failure in pneumonia. Arch Dis Child 2008; 93:221.
  65. Clifford V, Tebruegge M, Vandeleur M, Curtis N. Question 3: can pneumonia caused by penicillin-resistant Streptococcus pneumoniae be treated with penicillin? Arch Dis Child 2010; 95:73.
  66. Friedland IR. Comparison of the response to antimicrobial therapy of penicillin-resistant and penicillin-susceptible pneumococcal disease. Pediatr Infect Dis J 1995; 14:885.
  67. Pírez MC, Martínez O, Ferrari AM, et al. Standard case management of pneumonia in hospitalized children in Uruguay, 1997 to 1998. Pediatr Infect Dis J 2001; 20:283.
  68. Kaplan SL, Barson WJ, Lin PL, et al. Continued decline in invasive pneumococcal infections in children among 8 children's hospitals in the United States 2011 to 2013. https://idsa.confex.com/idsa/2014/webprogram/Paper45148.html (Accessed on November 17, 2014).
  69. Centers for Disease Control and Prevention. ABCs Report: Streptococcus pneumoniae, 2013. www.cdc.gov/abcs/reports-findings/survreports/spneu13.html (Accessed on November 17, 2014).
  70. Pelton SI, Huot H, Finkelstein JA, et al. Emergence of 19A as virulent and multidrug resistant Pneumococcus in Massachusetts following universal immunization of infants with pneumococcal conjugate vaccine. Pediatr Infect Dis J 2007; 26:468.
  71. Moore MR, Gertz RE Jr, Woodbury RL, et al. Population snapshot of emergent Streptococcus pneumoniae serotype 19A in the United States, 2005. J Infect Dis 2008; 197:1016.
  72. Bradley JS, Arguedas A, Blumer JL, et al. Comparative study of levofloxacin in the treatment of children with community-acquired pneumonia. Pediatr Infect Dis J 2007; 26:868.
  73. Feikin DR, Schuchat A, Kolczak M, et al. Mortality from invasive pneumococcal pneumonia in the era of antibiotic resistance, 1995-1997. Am J Public Health 2000; 90:223.
  74. Fitzwater SP, Chandran A, Santosham M, Johnson HL. The worldwide impact of the seven-valent pneumococcal conjugate vaccine. Pediatr Infect Dis J 2012; 31:501.
  75. Olarte L, Barson WJ, Barson RM, et al. Pneumococcal pneumonia requiring hospitalization in US children in the 13-valent pneumococcal conjugate vaccine era (abstract). 9th World Congress of The World Society for Pediatric Infectious Diseases (WSPID), Rio de Janeiro, Brazil. November 2015.
  76. Cutts FT, Zaman SM, Enwere G, et al. Efficacy of nine-valent pneumococcal conjugate vaccine against pneumonia and invasive pneumococcal disease in The Gambia: randomised, double-blind, placebo-controlled trial. Lancet 2005; 365:1139.
Topic 6060 Version 32.0

References

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