Version May 2024
INTRODUCTION — Streptococcus pneumoniae (pneumococcus) has long been one of the most prominent bacterial causes of disease in humans and was one of the first to be identified as a cause of human infection [1]. Since 2000, however, its impact has been blunted by the widespread use of vaccines that largely prevent infection and colonization in young children.
This topic will discuss the epidemiology, risk factors, clinical syndromes, and the general principles of treatment of invasive pneumococcal disease in adults. Microbiology and pathogenesis of Streptococcus pneumoniae are discussed separately (see "Streptococcus pneumoniae: Microbiology and pathogenesis of infection"). Treatment considerations specific to the site of infection (eg, pneumonia, meningitis, endocarditis, septic arthritis) are discussed in detail elsewhere (see "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Patients who respond to therapy' and "Treatment of bacterial meningitis caused by specific pathogens in adults", section on 'Streptococcus pneumoniae' and "Antimicrobial therapy of left-sided native valve endocarditis", section on 'Streptococcus pneumoniae' and "Septic arthritis in adults", section on 'Treatment'). Vaccination against pneumococcal disease in adults and children are discussed elsewhere. (See "Pneumococcal vaccination in adults" and "Pneumococcal vaccination in children" and "Pneumococcal immunization in adults with HIV".)
EPIDEMIOLOGY — S. pneumoniae is strictly a human pathogen, although animal models have been created to study the disease. Some genetic features have been associated with susceptibility to invasive pneumococcal disease (IPD), but the mechanism(s) underlying the association remain unknown [2].
A single nasopharyngeal culture shows about 20 to 25 percent of children in the United States to be colonized; with repeated sampling, the prevalence rises to 30 to 40 percent and, in daycare settings, it exceeds 50 percent [3]. On any single occasion, about 5 to 10 percent of adults are colonized; these rates have not changed substantially since introduction of the conjugate polysaccharide pneumococcal vaccine [4]. As might be expected, the rate of colonization is greater in parents of young children and lower in adults who have no exposure to children.
IPD in adults occurs more frequently from October through March than in May, June, or September and is rare in July and August [5,6]. The mechanism behind this seasonal variation remains unknown.
RISK FACTORS FOR INVASIVE DISEASE — There are many risk factors for invasive pneumococcal disease (IPD). The most important risk factors are discussed below (table 1).
●Effect of colonization – Colonization, a condition in which pneumococci persist on mucosal surfaces in the upper respiratory tract without causing symptoms, is an actively immunizing process. Dendritic cells take in and process pneumococcal antigens and then present them to appropriate B cells. Within a few weeks of becoming colonized by pneumococci, healthy children [7] and adults [8] develop antibodies to the capsular polysaccharide. When invasive disease occurs, it is most likely to do so in the time between colonization and appearance of antibodies. Persons who have diminished capacity to produce antibodies to capsular polysaccharides remain susceptible while they are colonized. Conditions that affect the ability to mount an antibody response to S. pneumoniae are listed in the table (table 1).
●Effect of age – In adults, the incidence of and mortality from IPD increases with advancing age (figure 1). The figure shows the incidence by age in the pre-antibiotic era [9], the late 1980s (before introduction of conjugate pneumococcal vaccine [10]), and after the widespread use of 7-valent pneumococcal conjugate vaccine and introduction of 13-valent conjugate vaccine [11]. Note, in each case, the change in the vertical scale, which shows a steady decline, since the 1980s, in the overall frequency of IPD in the population.
Levels and quality of antibody to capsular polysaccharides diminish with aging. With increased age, vaccinated persons produce lower levels of IgG, and the antibody has diminished effectiveness as an opsonizing agent [12,13]. These principles were illustrated in a remarkable case-control study showing that, with aging, the protective efficacy of pneumococcal polysaccharide vaccine (PPSV) was lower and declined more rapidly with time from vaccination, such that almost no protection was demonstrated in adults over 80 years of age [14].
●Effect of race and ethnicity – In the United States, IPD is more common in self-identified Black people [15-17] and Native Americans [18-20] than in persons who identify as part of the White population. Although socioeconomic factors [15] and comorbidities [18] certainly contribute [21], there is thought to be a distinct genetic basis, but the mechanism(s) underlying these predispositions is unknown.
●Crowded living arrangements – Crowding, whether among miners in South Africa [22], soldiers in military barracks [23,24], prisoners [25], or persons living in homeless shelters [26], is highly associated with increased risk and even outbreaks of pneumococcal disease. The increased risk of IPD in some of these groups is striking; a population-based study from Toronto [27] showed a 30-fold increase in the risk of IPD among homeless persons compared with the population at large. It remains unknown what causes crowding to increase the risk of pneumococcal disease although several theories have been proposed. For example, some studies have found physical and emotional stress to be related to susceptibility to IPD among military recruits in the Second World War [23,24].
●Immunocompromising conditions – Adults who acquire conditions that prevent them from making antibody to new antigens are at high risk for IPD (table 1). Patients with multiple myeloma or lymphoma are especially unable to make antibody in response to polysaccharide antigens. IPD appears regularly in patients with untreated lymphoma or multiple myeloma and, in fact, often leads to the initial recognition of these conditions [28,29].
An extensive literature has amply documented the susceptibility of patients with human immunodeficiency virus (HIV) to IPD. Early in the acquired immunodeficiency syndrome (AIDS) era, the incidence of bacteremic pneumococcal pneumonia was increased 200-fold over that in an age-matched population [30], and a more recent study of adults ages 18 to 64 years showed that the rate of IPD was 46 times greater among patients with AIDS than among those without known HIV infection [16]. Antiretroviral treatment reduces this risk but, despite such treatment, the incidence of IPD remains sevenfold greater in patients with HIV than in the general population [31].
●Comorbidities – Frailty and comorbid conditions probably contribute more to susceptibility to IPD than does simple chronologic age [32]. Chronic pulmonary disease is the most common condition that predisposes to IPD; other conditions are listed in the table (table 1) [33]. Other individuals with abnormal polymorphonuclear function or conditions with multifactorial effects such as malnutrition, alcoholism, cirrhosis, and chronic renal disease are also susceptible to IPD.
Diabetes mellitus is associated with IPD; in two population-based studies, the risk of IPD in people with diabetes was six times greater than that in the population at large [17,34]. Impaired function of polymorphonuclear leukocytes (PMNs) is likely responsible. However, in a homogeneous Danish population, the risk was increased but at a much lower rate [35]. A multicenter study found that diabetes was the only comorbid condition of many that were examined that was specifically associated with increased mortality from IPD in patients hospitalized in an intensive care unit [36]. It is not clear whether risk from diabetes remains if the diabetes is well controlled, although studies in vitro specifically show that diminished PMN function is specifically related to increased levels of glucose (table 1).
The strong association between alcohol ingestion and IPD has been noted since the beginning of the 20th century [9], and a >10-fold risk of IPD in persons with alcohol abuse syndrome continues to the present time [17]. The broad range of adverse effects of alcohol on the immune system, from suppression of innate immunity to altered cytokine responses, have been examined in depth elsewhere [37].
Hyposplenism is a major risk factor for IPD. Slow flow of blood through the sinusoids of Billroth enables clearance of bacteria, even encapsulated ones, in the absence of antibody. Splenectomy, hyposplenism, and poor splenic function because of hemoglobinopathy are all highly associated with overwhelming pneumococcal bacteremia [38,39].
Systemic lupus erythematosus, even in the absence of corticosteroid therapy, also carries increased risk of IPD [40].
CLINICAL SYNDROMES — Most of the important observations on the manifestations of invasive pneumococcal disease (IPD) cited in this section are derived from the century of study that preceded the widespread use of pneumococcal vaccine.
Spectrum of disease — IPD is defined as infection in which S. pneumoniae is isolated from a normally sterile body site. Specific presentations of IPD to be discussed in this section are listed in the approximate order of decreasing frequency in the table (table 2).
Bacteremic pneumococcal pneumonia with or without empyema is, by far, the most common presentation, followed by pneumococcal bacteremia in which no source is identified (termed "primary pneumococcal bacteremia"). Meningitis, septic arthritis, spontaneous peritonitis, osteomyelitis, endocarditis, and soft tissue infection are other major forms of IPD.
Bacteremic pneumococcal pneumonia and empyema — Pneumonia is the most common source of IPD, identified in 65 to 85 percent of invasive pneumococcal cases [6,41,42]. Presumptive pneumococcal pneumonia is the isolation of S. pneumoniae only from sputum. Proven pneumococcal pneumonia requires isolation of S. pneumoniae from either the blood or another normally sterile body site.
Bacteremia is documented in about 20 to 25 percent of cases of pneumococcal pneumonia [9,43]. Patients with positive blood cultures tend to be younger, present with a shorter period of illness, and have a higher likelihood of severe disease including septic shock, in-hospital mortality, and 30-day mortality [44-46]. In bacteremic individuals, the mortality is proportional to the initial severity of infection [47], and the risk has been shown to persist for 10 years [47,48]. (See 'Prognosis and prevention' below.)
Patients with bacteremic pneumococcal pneumonia often present with a dense lobar consolidation [44,49,50], and white blood cell (WBC) counts <6000 or >25,000 are associated with five- and threefold greater mortality, respectively [51].
Empyema occurs in about 5 percent of patients with bacteremic pneumococcal pneumonia. Organisms may reach the pleural space either by extension of pneumonia to the visceral pleura or by bacteremia with pneumococci settling in an area of compromised immunity (pneumococcal peritonitis). We evaluate for empyema in every patient with invasive pneumococcal pneumonia who does not respond to antibiotic therapy within a few days [9]. (See "Pneumococcal pneumonia in patients requiring hospitalization", section on 'Pleural effusion and empyema'.)
The clinical manifestations, diagnosis, and treatment of bacteremic pneumococcal pneumonia are discussed in detail separately. (See "Pneumococcal pneumonia in patients requiring hospitalization".)
Bacteremia of unknown source — Bacteremia with no recognizable source, also known as primary bacteremia, has been reported in about 5 to 20 percent of cases of IPD. In these circumstances, we perform a thorough history and examination and tailor further diagnostic tests based on present symptoms or signs that may indicate another site of infection (eg, computed tomography [CT] of abdomen and pelvis for abdominal pain). (See 'Further evaluation for other sites of infection' below.)
In one intensive prospective study using more modern techniques, only 5.1 percent of patients with IPD had bacteremia of unknown source [42].
Meningitis — In the absence of an outbreak of meningococcal meningitis, S. pneumoniae remains the most common cause of bacterial meningitis at all ages and in all groups of patients except neonates [52,53].
No distinctive clinical features or findings in the cerebrospinal fluid (CSF) other than Gram stain and culture enable pneumococcal meningitis to be distinguished from that due to other bacterial causes. Blood cultures are usually, but not always, positive. CSF contains hundreds to thousands of WBCs per microL, the glucose level is very low (usually <25 mg/dL), and the protein is likely to exceed 200 mg/dL. Before antibiotics are administered, large numbers of bacteria (>107 per mL) are regularly present [54]. If lumbar puncture is done before or soon after antibiotics are begun, Gram stain of centrifuged CSF should lead to the correct diagnosis in >95 percent of cases [55]. After 12 to 18 hours of antibiotics, pneumococci may no longer be cultured from CSF and the cell count and protein may be difficult to interpret, supporting the need for urgent spinal tap if meningitis is suspected.
Further details on epidemiology, clinical manifestations, diagnosis, management, and neurological complications of pneumococcal meningitis are discussed elsewhere. (See "Epidemiology of community-acquired bacterial meningitis in adults" and "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Initial therapy and prognosis of community-acquired bacterial meningitis in adults" and "Treatment of bacterial meningitis caused by specific pathogens in adults", section on 'Streptococcus pneumoniae' and "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults".)
Pneumococcal peritonitis (intraabdominal infection) — Pneumococcal peritonitis can be categorized into three broad categories: (1) peritonitis occurring in persons who had pre-existing ascites, (2) peritonitis following a gastric phlegmon or perforated viscus, or (3) peritonitis in females, occurring from ascent of pneumococci via the Fallopian tubes [56].
●Spontaneous bacterial peritonitis in patients with ascites – Spontaneous pneumococcal peritonitis in patients with pre-existing ascites occurs in both males and females. In persons who have pre-existing ascites, the peritoneal cavity serves as a compromised site (locus minoris resistentiae), and pneumococci lodge there during recognized or unrecognized bacteremia. This condition is called primary pneumococcal peritonitis. In the preantibiotic era, a small proportion of patients with pneumococcal pneumonia developed peritonitis as a complication; it is not certain whether all of these had pre-existing ascites. (See "Spontaneous bacterial peritonitis in adults: Clinical manifestations" and "Spontaneous bacterial peritonitis in adults: Diagnosis" and "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis".)
●Peritonitis associated with perforation – Secondary pneumococcal peritonitis in males or females follows perforation of a viscus, such as a gastric or duodenal ulcer, acute appendicitis, or cholecystitis, or is associated with gastric phlegmon. Pathogenesis is presumed to be the ingestion of pneumococci in the absence of antibody. In some cases, the pathogenesis is simply obscure [57].
●Peritonitis associated with the female genital tract – In the absence of pre-existing ascites or perforation/infection of a viscus, pneumococcal peritonitis occurs almost exclusively in females; the pathogenesis in these cases is ascent via the female genital tract. In this third scenario, most cases occur post-partum, in association with an intrauterine device, or following a syndrome of pelvic inflammatory disease [58-60]. When pneumococcal peritonitis occurs in females with none of these known predisposing conditions, an unrecognized underlying infection of the genital tract is thought to be responsible, and patients should be evaluated for this. (See "Postpartum endometritis" and "Intrauterine contraception: Management of side effects and complications" and "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)
Septic arthritis — Septic arthritis occurs in about 1.5 percent of IPD cases, and S. pneumoniae is the third most common bacterial cause of septic arthritis [61-63]. Most adults with pneumococcal septic arthritis have predisposing rheumatologic conditions, such as rheumatoid arthritis, osteoarthritis, gout or pseudogout, and/or alcohol use disorder [61,64]. Although any large joint may be affected, the knee, alone or together with other joints, is involved in more than one-half of all cases, perhaps because of associated daily trauma. Prosthetic knee joints are also susceptible to pneumococcal infection [65]. Polyarthritis, detected in 56 percent of cases, is more common in pneumococcal septic arthritis than in that due to other bacteria, perhaps related to the high proportion (70 percent) of patients who have documented bacteremia. Primary bacteremia or endocarditis rather than pneumonia is often the cause of pneumococcal arthritis or osteomyelitis [42,66].
Endocarditis — Pneumococcal endocarditis occurs rarely with one or two cases being seen each decade in large tertiary care hospitals; 16 cases were documented in the entire country of Denmark during a 12-year period [42,67,68]. The disease has a particularly high association with alcohol abuse syndrome. The majority of cases follow pneumonia and involve previously normal valves, although previously diseased or prosthetic valves may also be infected. Pneumococcal endocarditis is usually fulminant with a high rate of embolic complications, perforation, and need for valve replacement. Often, infection is present at multiple body sites. Of 30 patients with pneumococcal endocarditis, 10 underwent spinal tap, of whom 9 had findings consistent with meningitis. (See "Antimicrobial therapy of left-sided native valve endocarditis", section on 'Streptococcus pneumoniae' and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis" and "Right-sided native valve infective endocarditis" and "Native valve endocarditis: Epidemiology, risk factors, and microbiology".)
Austrian syndrome — Robert Austrian, an American expert on S. pneumoniae, described eight patients, seen between 1946 and 1954, who had pneumococcal endocarditis, pneumonia, and meningitis [2]. Originally called Osler's triad, this syndrome was renamed to honor Dr. Austrian. In more recent years, the syndrome occurs infrequently but remains lethal in many cases.
Pericarditis — Pneumococcal pericarditis has been described only rarely in the antibiotic era [69], although this condition occurred more frequently with pneumococcal pneumonia and especially as a complication of endocarditis in the preantibiotic era. The presentation may be as pericarditis or pericarditis with tamponade [70]. (See "Etiology of pericardial disease", section on 'Bacterial' and "Acute pericarditis: Clinical presentation and diagnosis".)
Miscellaneous infections — Pneumococcal osteomyelitis in adults tends to involve the vertebral bodies [66,71]. Spinal epidural abscess was reported as a complication in one-half of cases [66]. Brain abscesses have been rare in the antibiotic era [72]. Soft tissue infections may occur in persons who have connective tissue diseases or HIV infection [73,74]. Bacteremia leading to cellulitis has been described as a complication of pneumonia, generally occurring in patients who have severe underlying diseases [75].
DIAGNOSTIC EVALUATION
When to suspect IPD — Clinically, infections due to invasive pneumococcal disease (IPD) cannot be distinguished from those due to other bacterial pathogens that cause similar infectious syndromes. Nevertheless, IPD should be considered in patients presenting with sepsis without an apparent focus of infection, especially those who have underlying susceptibility to infection by encapsulated organisms such as patients without a functional spleen. Austrian syndrome should be suspected if a patient presents with respiratory and meningeal symptoms, and/or evidence of endocarditis.
Establishing the diagnosis — S. pneumoniae should always be considered a true pathogen when isolated from a sterile body site. The bacteria can be identified using routine, phenotype-based culture systems (see "Streptococcus pneumoniae: Microbiology and pathogenesis of infection", section on 'Microbiology'). Although urinary antigen detection is helpful in the diagnosis of pneumococcal pneumonia, its sensitivity for detecting pneumococcal invasive infection in the absence of pneumonia is around 60 percent [76]. Pneumococcal blood polymerase chain reaction (PCR) testing shows promise for detecting IPD but larger, more robust studies are needed prior to widespread clinical use [77,78].
POST-DIAGNOSTIC EVALUATION
Evaluation for underlying immunocompromise — In patients with invasive pneumococcal disease (IPD) without evident risk factors for invasive disease (eg, extremes of age, immunocompromising condition), we send HIV testing and immunoglobulin level testing to evaluate for immunocompromise.
Further evaluation for other sites of infection — Some patients develop pneumococcal infection at multiple sites throughout the course of infection. After diagnosis of IPD, we tailor further workup based on the patient's symptoms. We only perform a lumbar puncture if there is suspicion of meningitis based on the patient's mental status and other clinical neurological signs. Similarly, since pneumococcal endocarditis is rare, we do not perform transthoracic echocardiography in all patients with IPD; instead, we choose to proceed with transthoracic echocardiogram (TTE) in select cases where bacteremia is persistent (≥3 days), there is presence of a new heart murmur, and/or there is evidence of endocarditis stigmata.
TREATMENT
Overview — The goal of treatment is the eradication of infection. Treatment of invasive pneumococcal disease (IPD) consists of appropriate antibiotic treatment and drainage/debridement, when applicable.
Treatment of pneumococcal pneumonia, meningitis, and endocarditis is discussed separately. (See "Pneumococcal pneumonia in patients requiring hospitalization", section on 'Treatment' and "Treatment of bacterial meningitis caused by specific pathogens in adults", section on 'Streptococcus pneumoniae' and "Antimicrobial therapy of left-sided native valve endocarditis", section on 'Streptococcus pneumoniae'.)
Management of individual infections (eg, osteomyelitis, septic arthritis) is discussed in topics on each respective syndrome. (See "Septic arthritis in adults", section on 'Treatment' and "Nonvertebral osteomyelitis in adults: Treatment" and "Vertebral osteomyelitis and discitis in adults", section on 'Treatment' and "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis", section on 'Treatment' and "Purulent pericarditis", section on 'Treatment'.)
Antibiotic selection for nonmeningeal disease — Beta-lactam antibiotics are the mainstay of treatment. Although S. pneumoniae is not as susceptible to penicillin as it was in the preantibiotic era (table 3), beta-lactamase production has not been described, and the parenteral doses of penicillin, ampicillin, and ceftriaxone that are ordinarily prescribed provide effective therapeutic levels in nearly all cases of IPD.
For patients with a beta-lactam allergy, the severity and characteristics of the allergy should be assessed to determine whether the patient can receive penicillins, cephalosporins, or carbapenems (see "Choice of antibiotics in penicillin-allergic hospitalized patients"). For patients with serious penicillin allergies, carbapenems, fluoroquinolones, vancomycin, and linezolid are reasonable alternatives for treatment of IPD.
The susceptibility of pneumococci to various antibiotics is discussed in detail 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".)
Initial antibiotic regimen — Patients with IPD warrant initial treatment with intravenous or highly bioavailable oral antibiotics until they are clinically stable. We suggest ceftriaxone 1 to 2 g intravenously every 24 hours (1 g every 12 hours is preferred if the penicillin minimal inhibitory concentration [MIC] is ≥4 or unknown (table 3)) due to its excellent efficacy, ease of dosing, and affordability.
Penicillin G 2 million units intravenously every 4 hours (only if MIC <2 mcg/mL (table 3)) is also a reasonable option.
Alternative options for patients who cannot tolerate penicillins or cephalosporins include:
●Levofloxacin 750 mg intravenously or orally every 24 hours
●Moxifloxacin 400 mg intravenously or orally every 24 hours
●Vancomycin intravenously (table 4 and table 5)
●Linezolid 600 mg intravenously or orally every 12 hours
Pneumococcal susceptibility to the alternative agents used should be confirmed with the microbiology laboratory.
Oral step-down regimens in select cases — After the first few doses in a stable patient, there is no need to give antibiotics intravenously except in endovascular (eg, endocarditis) infections or meningitis and rare cases in which a particularly high MIC mandates it (table 3) [79]. Oral step-down regimens (once microbiological susceptibility is confirmed) include:
●Amoxicillin 1 g every 8 hours (only if MIC <2 mcg/mL (table 3))
●Cefuroxime axetil 500 mg orally every 12 hours
●Levofloxacin 750 mg orally every 24 hours
●Moxifloxacin 400 mg orally every 24 hours
●Linezolid 600 mg orally every 12 hours
Duration of therapy — The duration of therapy depends on the underlying site of infection. In general, antimicrobial therapy should be administered until clinical signs of infection have resolved and as recommended for the site of infection.
The duration of treatment for primary pneumococcal bacteremia remains unclear. In the absence of good data, we prefer to treat bacteremic pneumococcal pneumonia for five to seven days and isolated bacteremia without evidence of pneumonia for 8 to 10 days.
PROGNOSIS AND PREVENTION — The estimated case fatality rate for pneumococcal bacteremia among adults is around 20 to 30 percent [80-85] and can be as high as 60 percent in patients with certain factors, such as older age or the presence of comorbid conditions (eg, asplenia or immunocompromising conditions, alcohol abuse) (figure 2). The degree of severity of infection and the pneumococcal serotype causing the infection also affect the mortality rate. For patients that do survive, long-lasting morbidity can be a problem. An increased rate of death persists for up to 10 years after pneumococcal bacteremia [47]; lasting epigenetic changes may be responsible [86]. For pneumococcal septic arthritis, many patients are left with residual dysfunction in the joint [87].
Vaccination is the most effective means of preventing pneumococcal infection and is discussed separately (see "Pneumococcal vaccination in adults" and "Pneumococcal immunization in adults with HIV"). Other preventive measures include smoking cessation, limiting alcohol intake, and optimizing care of predisposing conditions, such as asthma or chronic obstructive pulmonary disease (COPD).
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: Community-acquired pneumonia in adults" and "Society guideline links: Bacterial meningitis in adults" and "Society guideline links: Bacterial meningitis in infants and children" and "Society guideline links: Pneumococcal vaccination in adults".)
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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 info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Sepsis in adults (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition of invasive pneumococcal disease – Invasive pneumococcal disease (IPD) refers to an infection caused by S. pneumoniae in a normally sterile body site, such as blood, cerebrospinal fluid (CSF), pleural fluid, synovial fluid, or pericardial fluid. (See 'Introduction' above and 'Spectrum of disease' above.)
●Epidemiology and risk factors – S. pneumoniae is strictly a human pathogen. Risk factors include colonization, extremes of age, frailty, race and ethnicity, crowded living arrangements, and immunocompromising conditions and other medical comorbidities (table 1). (See 'Epidemiology' above and 'Risk factors for invasive disease' above.)
●Clinical manifestations – Bacteremic pneumococcal pneumonia with or without empyema is, by far, the most common presentation, followed by pneumococcal bacteremia in which no source is identified (termed "primary pneumococcal bacteremia") (table 2). (See 'Clinical syndromes' above.)
●Diagnostic evaluation – Clinically, invasive pneumococcal infections cannot be distinguished from other bacterial pathogens that cause similar infectious syndromes. S. pneumoniae should always be considered a true pathogen when isolated from a sterile body site. Pneumococcal urinary antigen and blood polymerase chain reaction (PCR) testing are not useful in the diagnosis of IPD. (See 'Diagnostic evaluation' above.)
●Post-diagnostic evaluation – After establishing the diagnosis of IPD, further evaluation is dependent on the patient's symptoms and signs on physical exam. If the patient does not have any evident risk factors for IPD, we send HIV and immunoglobulin testing to evaluate for immunocompromise. (See 'Post-diagnostic evaluation' above.)
●Treatment – The goal of treatment is the eradication of infection via appropriate antibiotic treatment and drainage/debridement, when applicable. Beta-lactam antibiotics are the mainstay of treatment. For patients with serious allergic reactions to penicillins, alternatives include carbapenems, fluoroquinolones, vancomycin, and linezolid. Pneumococcal susceptibility to the alternative agents used should be confirmed with the microbiology laboratory. (See 'Treatment' above.)
•Initial intravenous regimen – We suggest ceftriaxone 1 to 2 g intravenously every 24 hours (1 g every 12 hours is preferred if the penicillin minimum inhibitory concentration [MIC] is ≥4 or unknown (table 3)) due to its excellent efficacy, ease of dosing, and affordability (Grade 2C). (See 'Initial antibiotic regimen' above.)
•Oral step down regimens – After the first few doses in a stable patient, there is no need to give antibiotics intravenously except in endovascular (eg, endocarditis) and meningitis infections and rare cases in which a particularly high MIC mandates it (table 3) (see 'Oral step-down regimens in select cases' above). Oral step-down regimens (when microbiologic susceptibility is confirmed) include:
-Amoxicillin 1 g every 8 hours (only if MIC <2 mcg/mL (table 3))
-Cefuroxime axetil 500 mg orally every 12 hours
-Levofloxacin 750 mg orally every 24 hours
-Moxifloxacin 400 mg orally every 24 hours
-Linezolid 600 mg orally every 12 hours
•Duration of antibiotic therapy – The duration of therapy depends on the underlying site of infection. In general, antimicrobial therapy should be administered until clinical signs of infection have resolved and as recommended for the site of infection. (See 'Duration of therapy' above.)
●Prevention – Pneumococcal vaccination is the most effective means of preventing IPD. Other preventive measures include smoking cessation and optimizing care of predisposing conditions such as asthma and chronic obstructive pulmonary disease (COPD). (See 'Prognosis and prevention' above and "Pneumococcal vaccination in adults" and "Pneumococcal vaccination in children".)
ACKNOWLEDGMENT — UpToDate gratefully acknowledges John G Bartlett, MD (deceased), who contributed on earlier versions of this topic and was a founding Editor-in-Chief for UpToDate in Infectious Diseases.
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