Streptococcus pneumoniae (pneumococci) are gram-positive, alpha-hemolytic, aerobic, encapsulated diplococci. Pneumococcal infection is a major cause of otitis media, pneumonia, sepsis, meningitis, and death. Diagnosis is based on Gram stain and culture. Treatment depends on the resistance profile and location of infection and includes either a beta-lactam, a macrolide, doxycycline, omadacycline, a newer fluoroquinolone, or (pneumococci) are gram-positive, alpha-hemolytic, aerobic, encapsulated diplococci. Pneumococcal infection is a major cause of otitis media, pneumonia, sepsis, meningitis, and death. Diagnosis is based on Gram stain and culture. Treatment depends on the resistance profile and location of infection and includes either a beta-lactam, a macrolide, doxycycline, omadacycline, a newer fluoroquinolone, orvancomycin.
Pneumococci are fastidious, encapsulated microorganisms that require catalase to grow on agar plates. In the laboratory, pneumococci are identified by:
Gram-positive lancet-shaped diplococci
Catalase-negativity
Alpha-hemolysis on blood agar
Sensitivity to optochin
Lysis by bile salts
Pneumococci commonly colonize the human respiratory tract, particularly in winter and early spring. Spread occurs via airborne droplets.
True epidemics of pneumococcal infections are rare; however, some serotypes seem to be associated with outbreaks in certain populations or settings (eg, military, congregate settings, people who are homeless), particularly in crowded settings.
Serotypes
The pneumococcal capsule consists of a complex polysaccharide that determines serologic type and contributes to virulence and pathogenicity. Virulence varies somewhat within serologic types because of genetic diversity.
The pneumococcal capsule consists of a complex polysaccharide that determines serologic type and contributes to virulence and pathogenicity. Virulence varies somewhat within serologic types because of genetic diversity. The pneumococcal polysaccharide capsule is critical for evading phagocytosis.
More than 100 different pneumococcal serotypes have been identified based on their reaction with type-specific antisera (1).
The serotypes of pneumococci that colonize the nasopharynx vary by patient age and geographic location and have changed over time. Those serotypes that colonize the nasopharynx, which are more heavily encapsulated and tend to form more mucoid colonies than other serotypes, are more often associated with invasive pneumococcal disease in patients.
The serotypes responsible for most serious infections (serotypes 3, 4, 6B, 9V, 14, 18C, 19F, and 23F) cause about 90% of invasive infections in children and up to 85% in adults (2). These serotypes are contained in current pneumococcal conjugate vaccines to bolster immunity to them. In part because of the widespread use of polyvalent vaccines, the most prevalent serotypes are changing.
Serotype 19A, which is highly virulent and multidrug-resistant, has emerged as an important cause of respiratory tract infection and invasive disease.
Pneumococcal conjugate vaccines protect against various infection-causing serotypes (eg, the updated PCV21-valent pneumococcal conjugate vaccine includes 8 unique serotypes that cause approximately 20 to 30% of invasive pneumococcal disease [3]). A 23-valent pneumococcal polysaccharide vaccine (PPSV23) offers strong protection against invasive pneumococcal disease, including bacteremia and meningitis, but it is not as effective in preventing pneumonia.
Risk factors for pneumococcal infection
Patients most susceptible to serious and invasive pneumococcal infections include young children (< 5 years), older adults (> 65 years) and individuals with one or more of the following characteristics:
Chronic illness (eg, chronic cardiorespiratory disease, diabetes, liver disease, alcohol use disorder)
Immunodeficiency or immunosuppression (eg, HIV, congenital and acquired hypogammaglobulinemia [such as from multiple myeloma], complement pathway deficiencies, neutropenia, immunosuppressant medications, radiation therapy, solid organ transplants)
Congenital or acquired asplenia (due to an inability to eradicate encapsulated organisms)
Sickle cell disease or other hemoglobinopathies
Cigarette smoking
Chronic kidney disease or nephrotic syndrome
Cochlear implant
Cerebrospinal fluid leak
Malignancy (eg, generalized cancer, Hodgkin disease, leukemia, lymphoma)
Being residents of long-term care facilities or being an Australian or Pacific Islander of Aboriginal ancestry, an Alaskan native, or descended from certain groups of American Indians
Older adults, even those without chronic conditions, tend to have a poor prognosis with pneumococcal infections.
Damage to the respiratory epithelium by chronic bronchitis or common respiratory viral infections, notably influenza, may predispose to pneumococcal invasion.
General references
1. Camargo DR, Pais FS, Volpini ÂC, Oliveira MA, Coimbra RS. Revisiting molecular serotyping of Streptococcus pneumoniae. BMC Genomics. 2015;16 Suppl 5(Suppl 5):S1. doi:10.1186/1471-2164-16-S5-S1
2. Weir E. Streptococcus pneumoniae infection in children: vaccine implications. CMAJ. 2002;166(2):220.
3. Kobayashi M, Leidner AJ, Gierke R, et al. Use of 21-Valent Pneumococcal Conjugate Vaccine Among U.S. Adults: Recommendations of the Advisory Committee on Immunization Practices - United States, 2024. MMWR Morb Mortal Wkly Rep. 2024;73(36):793-798. Published 2024 Sep 12. doi:10.15585/mmwr.mm7336a3
Diseases Caused by Pneumococci
Pneumococcal diseases include:
Primary pneumococcal infection usually involves the sinuses, middle ear, or lungs.
The diseases listed below are further discussed elsewhere in The Manual.
Pneumococcal acute otitis media
Acute otitis media in infants (after the neonatal period) and children is caused by pneumococci in approximately 20% of cases (1). Approximately 40% of children in most populations develop acute pneumococcal otitis media during the first 2 years of life, and pneumococcal otitis media commonly recurs (2). Relatively few serotypes of S. pneumoniae are responsible for most cases. After universal immunization of infants in the United States beginning in 2000, the relative contribution of S. pneumoniae (particularly serotype 19A, which was not in the original protein-conjugated pneumococcal vaccine) to acute otitis media has declined, and serotypes causing it have shifted to include those for which vaccination does not provide immunity. (particularly serotype 19A, which was not in the original protein-conjugated pneumococcal vaccine) to acute otitis media has declined, and serotypes causing it have shifted to include those for which vaccination does not provide immunity.
Complications include:
Mild conductive hearing loss
Vestibular balance dysfunction
Tympanic membrane perforation
Mastoiditis
Petrositis
Labyrinthitis
Intracranial complications are rare in high-resource countries but may include meningitis, epidural abscess, brain abscess, lateral venous sinus thrombosis, cavernous sinus thrombosis, subdural empyema, and carotid artery thrombosis.
Pneumococcal pneumonia
Pneumonia is the most frequent serious infection caused by pneumococci; it may manifest as lobar pneumonia or, less commonly, as bronchopneumonia. Millions of cases of community-acquired pneumonia occur each year in the United States; when community-acquired pneumonia requires hospitalization, pneumococci are the most common bacterial etiologic agent in patients of all ages.
Pleural effusion occurs in approximately 50% of patients, but most effusions resolve during pharmacotherapy (3). Only approximately 5% of patients develop complicated pleural effusions, including empyema (3, 4), which may become loculated, thick, and fibrinopurulent; empyema has been most commonly associated with S. pneumoniae serotype 1. Lung abscesses due to S. pneumoniae occur more frequently in children; serotype 3 is the usual pathogen, but other pneumococcal serotypes may be involved.
Pneumococcal paranasal sinusitis
Paranasal sinusitis may be caused by pneumococci and may become chronic and polymicrobic.
Most commonly, the maxillary and ethmoid sinuses are affected. Infection of the sinuses causes pain and purulent discharge and may extend into the cranium, causing the following complications:
Cavernous sinus thrombosis
Brain, epidural, or subdural abscesses
Septic cortical thrombophlebitis
Meningitis
Pneumococcal bacteremia
Pneumococcal bacteremia can occur in immunocompetent and immunosuppressed patients; patients who have had splenectomy are at particular risk.
Bacteremia may be the primary infection, or it may accompany the acute phase of any focal pneumococcal infection. Pneumococcal bacteremia can be complicated by sepsis and septic shock. When bacteremia is present, secondary seeding of distant sites may cause infections such as septic arthritis, meningitis, and endocarditis.
Despite treatment, the overall case-fatality rate for pneumococcal bacteremia is about 20% but may be as high as 60% among older adults (1).
The risk of death is highest during the first 3 days of bacteremia.
Pneumococcal meningitis
Acute purulent meningitis is frequently caused by pneumococci and may be secondary to bacteremia resulting from other infected foci (notably pneumonia); direct extension from infection of the ear, mastoid process, or paranasal sinuses; or basilar fracture of the skull involving one of these sites or the cribriform plate (usually with cerebrospinal fluid leakage), thus giving bacteria in the paranasal sinuses, nasopharynx, or middle ear access to the central nervous system.
Typical meningitis symptoms (eg, headache, stiff neck, fever) occur.
Complications after pneumococcal meningitis occur in up to 50% of patients (1) and may include:
Hearing loss
Seizures
Intellectual disabilities
Behavioral disabilities
Motor deficits
Pneumococcal endocarditis
Acute bacterial endocarditis (a rapidly progressing subtype of infective endocarditis), may rarely result from pneumococcal bacteremia, even in patients without valvular heart disease.
Pneumococcal endocarditis may lead to the formation of corrosive valvular lesions, with associated sudden ruptures or fenestrations, leading to rapidly progressive heart failure and requiring urgent valve replacement. Austrian syndrome is a rare condition characterized by the triad of pneumococcal meningitis, pneumonia, and endocarditis due to S. pneumoniae and has a high fatality rate. Congenital aortic valve insufficiency is the most common cause of heart failure in affected patients.
Pneumococcal septic arthritis
Septic arthritis of pneumococcal origin, similar to that caused by other gram-positive cocci, is usually a complication of pneumococcal bacteremia from another focus of infection.
Spontaneous pneumococcal peritonitis
Spontaneous pneumococcal peritonitis occurs most often in patients with cirrhosis and ascites, with no features to distinguish it from spontaneous bacterial peritonitis of other causes.
Diseases caused by pneumococci references
1. Centers for Disease Control and Prevention (CDC). Pneumococcal Disease: Clinical Features of Pneumococcal Disease. February 6, 2024. Accessed July 18, 2025.
2. Kaur R, Morris M, Pichichero ME. Epidemiology of Acute Otitis Media in the Postpneumococcal Conjugate Vaccine Era [published correction appears in Pediatrics. 2018 Mar;141(3):e20174067. doi: 10.1542/peds.2017-4067.]. Pediatrics. 2017;140(3):e20170181. doi:10.1542/peds.2017-0181
3. Taryle DA, Potts DE, Sahn SA. The incidence and clinical correlates of parapneumonic effusions in pneumococcal pneumonia. Chest. 1978;74(2):170-173. doi:10.1378/chest.74.2.170
4. Light RW, Girard WM, Jenkinson SG, George RB. Parapneumonic effusions. Am J Med. 1980;69(4):507-512. doi:10.1016/0002-9343(80)90460-x
Diagnosis of Pneumococcal Infections
Gram stain and culture
Nucleic acid amplification test (NAAT) panels
Pneumococci are readily identified by their typical appearance on Gram stain as lancet-shaped diplococci. Gram staining and culture are the most commonly available and performed tests in most clinical settings. Culture confirms bacterial identification, and antimicrobial susceptibility testing reveals sensitivity patterns.
The characteristic capsule can be best detected using the Quellung test. In this test, application of antiserum followed by staining with India ink causes the capsule to appear like a halo around the organism. The pneumococcal capsule becomes visible microscopically after binding of the capsule with type-specific antiserum, which causes capsular swelling. After the addition of methylene blue, the pneumococcal cells stain dark blue and are surrounded by a sharply demarcated halo, which represents the outer edge of the capsule.The characteristic capsule can be best detected using the Quellung test. In this test, application of antiserum followed by staining with India ink causes the capsule to appear like a halo around the organism. The pneumococcal capsule becomes visible microscopically after binding of the capsule with type-specific antiserum, which causes capsular swelling. After the addition of methylene blue, the pneumococcal cells stain dark blue and are surrounded by a sharply demarcated halo, which represents the outer edge of the capsule.
Serotyping and genotyping of isolates can be helpful for epidemiologic reasons (eg, to follow the spread of specific clones and antimicrobial resistance patterns) (1). Differences in virulence within a serotype may be distinguished by techniques such as pulsed-field gel electrophoresis and multi-locus sequence typing.
Also gaining widespread acceptance in hospital settings, rapid molecular multiplex respiratory NAAT panels are very sensitive and specific for the detection of respiratory pathogens including S. pneumoniae (2). Positive NAAT from non-sterile upper respiratory tract specimens in young children must be correlated with the overall clinical picture as asymptomatic nasopharyngeal carriage is common.
The urine antigen detection test has high specificity (> 90%) but poor sensitivity (50 to 80%) and is greatly influenced by concurrent bacteremia (3). It is generally not recommended to be performed in young children because nasopharyngeal colonization can cause release of a bacterial cell wall polysaccharide that can enter the blood stream and be filtered by the kidney. The positive predictive value (the proportion of patients with a positive test that actually have the disease) is high (> 95%) in adults (4). However, the negative predictive value (the proportion of patients with a negative test that are actually disease free) is low, so a negative urine antigen test should not be used to exclude pneumococcal disease.
Diagnosis references
1. Self WH, Johnson KD, Resser JJ, et al. Prevalence, Clinical Severity, and Serotype Distribution of Pneumococcal Pneumonia Among Adults Hospitalized With Community-Acquired Pneumonia in Tennessee and Georgia, 2018-2022. Clin Infect Dis. 2024;79(4):838-847. doi:10.1093/cid/ciae316
2. Hanson KE, Azar MM, Banerjee R, et al. Molecular Testing for Acute Respiratory Tract Infections: Clinical and Diagnostic Recommendations From the IDSA's Diagnostics Committee. Clin Infect Dis. 2020;71(10):2744-2751. doi:10.1093/cid/ciaa508
3. Yasuo S, Murata M, Nakagawa N, et al. Diagnostic accuracy of urinary antigen tests for pneumococcal pneumonia among patients with acute respiratory failure suspected pneumonia: a systematic review and meta-analysis. BMJ Open. 2022;12(8):e057216. Published 2022 Aug 11. doi:10.1136/bmjopen-2021-057216
4. Laijen W, Snijders D, Boersma WG. Pneumococcal urinary antigen test: Diagnostic yield and impact on antibiotic treatment. Clin Respir J. 11(6):999–1005, 2017. doi: 10.1111/crj.12453
Treatment of Pneumococcal Infections
A beta-lactam, macrolide, respiratory fluoroquinolone (eg, levofloxacin, moxifloxacin), tetracycline (eg, ), tetracycline (eg,doxycycline, omadacycline), or pleuromutilin (eg, lefamulin)
Rarely, vancomycin Rarely, vancomycin
If pneumococcal infection is suspected, initial therapy pending susceptibility studies should be determined by local resistance patterns.
Although the preferred treatment for pneumococcal infections is a beta-lactam antibiotic, treatment is challenging because resistant strains have emerged. Strains highly resistant to penicillin, ampicillin, and other beta-lactams are common worldwide, and resistance rates vary geographically in the United States. The most common predisposing factor to beta-lactam resistance is use of these antibiotics within the past several months. Resistance to macrolide antibiotics has also increased significantly (approximately 35%) (Although the preferred treatment for pneumococcal infections is a beta-lactam antibiotic, treatment is challenging because resistant strains have emerged. Strains highly resistant to penicillin, ampicillin, and other beta-lactams are common worldwide, and resistance rates vary geographically in the United States. The most common predisposing factor to beta-lactam resistance is use of these antibiotics within the past several months. Resistance to macrolide antibiotics has also increased significantly (approximately 35%) (1); these antibiotics are not recommended as monotherapy for hospitalized patients with community-acquired pneumonia. Vancomycin may be added as an empiric treatment for suspected meningitis or other invasive disease until culture and sensitivity results are obtained and beta-lactam susceptibility is confirmed, at which point antibiotic coverage may be appropriately switched to beta-lactams.); these antibiotics are not recommended as monotherapy for hospitalized patients with community-acquired pneumonia. Vancomycin may be added as an empiric treatment for suspected meningitis or other invasive disease until culture and sensitivity results are obtained and beta-lactam susceptibility is confirmed, at which point antibiotic coverage may be appropriately switched to beta-lactams.
Susceptibility or resistance to beta-lactam antibiotics (penicillin and the extended-spectrum cephalosporins ceftriaxone and cefotaxime) depends on the site of infection and minimal inhibitory concentration (MIC) breakpoints. Administering higher dose beta-lactams can overcome potentially reduced antibiotic susceptibility in vivo encountered during the treatment of pneumonia and noninvasive infections. Susceptible organisms have MICs below the breakpoint, and resistant organisms have MICs above the breakpoint. MIC breakpoints are typically higher for nonmeningeal pneumococcal infection than for meningeal infection. Susceptibility or resistance to beta-lactam antibiotics (penicillin and the extended-spectrum cephalosporins ceftriaxone and cefotaxime) depends on the site of infection and minimal inhibitory concentration (MIC) breakpoints. Administering higher dose beta-lactams can overcome potentially reduced antibiotic susceptibility in vivo encountered during the treatment of pneumonia and noninvasive infections. Susceptible organisms have MICs below the breakpoint, and resistant organisms have MICs above the breakpoint. MIC breakpoints are typically higher for nonmeningeal pneumococcal infection than for meningeal infection.
Meningeal pneumococcal infections
MIC breakpoints for patients with meningeal pneumococcal infection:
Penicillin-susceptible strains: MIC ≤ 0.06 mcg/mL
Penicillin-resistant strains: MIC > 0.06 mcg/mL
Cefotaxime- and ceftriaxone-susceptible strains: MIC ≤ 0.5 mcg/mL
Cefotaxime- and ceftriaxone-intermediate strains: MIC > 0.5 to ≤ 1.0 mcg/mL
Cefotaxime- and ceftriaxone-resistant strains: MIC > 1.0 mcg/mL
If the penicillin MIC is ≤ 0.06 mcg/mL, treatment of meningeal pneumococcal infection may be with IV penicillin; however, ceftriaxone or cefotaxime is preferable.
If the penicillin MIC is > 0.06 mcg/mL and the ceftriaxone or cefotaxime MIC is ≤ 0.5 mcg/mL, treatment is with ceftriaxone or cefotaxime. MIC is ≤ 0.5 mcg/mL, treatment is with ceftriaxone or cefotaxime.
If the ceftriaxone or cefotaxime MIC is ≥ 1.0 mcg/mL, treatment is with ceftriaxone or cefotaxime plus vancomycin.MIC is ≥ 1.0 mcg/mL, treatment is with ceftriaxone or cefotaxime plus vancomycin.
Nonmeningeal pneumococcal infections
MIC breakpoints for patients with nonmeningeal pneumococcal infection:
Penicillin-susceptible strains: MIC ≤ 2 mcg/mL
Penicillin-intermediate strains: MIC > 2.0 to ≤ 4.0 mcg/mL
Penicillin-resistant strains: MIC > 4.0 mcg/mL
Cefotaxime- and ceftriaxone-susceptible strains: MIC ≤ 1 mcg/mL
Cefotaxime- and ceftriaxone-intermediate strains: MIC > 1.0 to ≤ 2.0 mcg/mL
Cefotaxime- and ceftriaxone-resistant strains: MIC > 2.0 mcg/mL
Seriously ill patients with nonmeningeal infections caused by organisms that are resistant to penicillin can often be treated with ceftriaxone or cefotaxime. High doses of parenteral penicillin G (eg, 20 to 40 million units/day IV for adults) also work, unless the MIC of the isolate is very high, indicating resistance.Seriously ill patients with nonmeningeal infections caused by organisms that are resistant to penicillin can often be treated with ceftriaxone or cefotaxime. High doses of parenteral penicillin G (eg, 20 to 40 million units/day IV for adults) also work, unless the MIC of the isolate is very high, indicating resistance.
Fluoroquinolones (eg, moxifloxacin, levofloxacin), doxycycline, omadacycline, and lefamulin are effective for respiratory infections with highly penicillin-resistant pneumococci in adults. Evidence suggests that the mortality rate for bacteremic pneumococcal pneumonia is lower when combination therapy (eg, macrolide plus beta-lactam) is used.Fluoroquinolones (eg, moxifloxacin, levofloxacin), doxycycline, omadacycline, and lefamulin are effective for respiratory infections with highly penicillin-resistant pneumococci in adults. Evidence suggests that the mortality rate for bacteremic pneumococcal pneumonia is lower when combination therapy (eg, macrolide plus beta-lactam) is used.
All penicillin-resistant isolates have been susceptible to vancomycin so far, but parenteral vancomycin does not always produce concentrations in cerebrospinal fluid adequate for treatment of meningitis (especially if glucocorticoids are also being used). Therefore, in patients with meningitis, ceftriaxone or cefotaxime is commonly used with vancomycin. To date, pneumococcal resistance to linezolid, daptomycin, and ceftaroline has not been demonstrated.. To date, pneumococcal resistance to linezolid, daptomycin, and ceftaroline has not been demonstrated.
Treatment reference
1. Suaya JA, Mendes RE, Sings HL, et al. Streptococcus pneumoniae serotype distribution and antimicrobial nonsusceptibility trends among adults with pneumonia in the United States, 2009‒2017. J Infect. 2020;81(4):557-566. doi:10.1016/j.jinf.2020.07.035
Prevention of Pneumococcal Infections
Infection produces type-specific immunity that does not generalize to other serotypes. Prevention involves:
Vaccination
Prophylactic antibiotics
Pneumococcal vaccines
See Pneumococcal Vaccine for more information, including indications, contraindications and precautions, dosing and administration, and adverse effects. See also the vaccine schedules for children and adolescents and for adults from the Centers for Disease Control and Prevention (CDC) and the pneumococcal vaccine recommendations from the Advisory Committee on Immunization Practices (ACIP) (. See also the vaccine schedules for children and adolescents and for adults from the Centers for Disease Control and Prevention (CDC) and the pneumococcal vaccine recommendations from the Advisory Committee on Immunization Practices (ACIP) (1, 2, 3).
Prophylactic antibiotics
For children < 5 years of age with functional or anatomic asplenia, prophylactic penicillin V orally 2 times a day is recommended. The duration for chemoprophylaxis is empiric, but some experts continue prophylaxis throughout childhood and into adulthood for high-risk patients with asplenia. Penicillin V orally 2 times a day is also recommended for older children or adolescents for at least 1 year after splenectomy.5 years of age with functional or anatomic asplenia, prophylactic penicillin V orally 2 times a day is recommended. The duration for chemoprophylaxis is empiric, but some experts continue prophylaxis throughout childhood and into adulthood for high-risk patients with asplenia. Penicillin V orally 2 times a day is also recommended for older children or adolescents for at least 1 year after splenectomy.
Prevention references
1. Centers for Disease Control and Prevention. Vaccines and Immunizations: Child and Adolescent Immunization Schedule by Age (Addendum updated July 2, 2025). July 2, 2025. Accessed July 21, 2025.
2. Centers for Disease Control and Prevention. Vaccines and Immunizations: Adult Immunization Schedule by Age (Addendum updated July 2, 2025). July 2, 2025. Accessed July 21, 2025.
3. Centers for Disease Control and Prevention. ACIP Vaccine Recommendations and Guidelines: ACIP Recommendations: Pneumococcal Vaccine. January 8, 2025. Accessed July 21, 2025. . ACIP Vaccine Recommendations and Guidelines: ACIP Recommendations: Pneumococcal Vaccine. January 8, 2025. Accessed July 21, 2025.
Key Points
Streptococcus pneumoniae (pneumococci) bacteria are gram-positive, alpha-hemolytic, aerobic, encapsulated diplococci.
Pneumococci cause many cases of otitis media and pneumonia and can also cause meningitis, sinusitis, endocarditis, and septic arthritis.
Patients with chronic respiratory tract disease or asplenia are at high risk of serious and invasive pneumococcal infections, as are patients who are immunocompromised.
Treat uncomplicated or mild outpatient infections with a beta-lactam, macrolide, doxycycline, or new fluoroquinolone antibiotic.Treat uncomplicated or mild outpatient infections with a beta-lactam, macrolide, doxycycline, or new fluoroquinolone antibiotic.
Because resistance to beta-lactam and macrolide antibiotics is increasing, seriously ill patients may be treated with an advanced-generation cephalosporin (eg, ceftriaxone or cefotaxime) based on minimal inhibitory concentration (MIC); other options include a respiratory fluoroquinolone (eg, moxifloxacin, levofloxacin), a tetracycline (eg, omadacycline), or a pleuromutilin (eg, lefamulin).Because resistance to beta-lactam and macrolide antibiotics is increasing, seriously ill patients may be treated with an advanced-generation cephalosporin (eg, ceftriaxone or cefotaxime) based on minimal inhibitory concentration (MIC); other options include a respiratory fluoroquinolone (eg, moxifloxacin, levofloxacin), a tetracycline (eg, omadacycline), or a pleuromutilin (eg, lefamulin).
Prevent pneumococcal infection in children 2 months through 6 years of age and in adults at high risk by giving pneumococcal vaccination.
Drugs Mentioned In This Article
