Streptococcus pneumoniae (Pneumococcus)

Etiology

Streptococcus pneumoniae is a gram-positive, lancet-shaped, polysaccharide encapsulated diplococcus, occurring occasionally as individual cocci or in chains; >90 serotypes have been identified by type-specific capsular polysaccharides. Antisera to some pneumococcal polysaccharides cross-react with other pneumococcal types, defining serogroups (e.g., 6A and 6B). Encapsulated strains cause most serious disease in humans. Capsular polysaccharides impede phagocytosis. Virulence is related in part to capsular size, but pneumococcal types with capsules of the same size can vary widely in virulence.

On solid media, S. pneumoniae forms unpigmented, umbilicated colonies surrounded by a zone of incomplete (α) hemolysis. S. pneumoniae is bile soluble (i.e., 10% deoxycholate) and optochin sensitive. S. pneumoniae is closely related to the viridans groups of Streptococcus mitis , which typically overlap phenotypically with pneumococci. The conventional laboratory definition of pneumococci continues to rely on bile and optochin sensitivity, although considerable confusion occurs in distinguishing pneumococci and other α-hemolytic streptococci. Pneumococcal capsules can be microscopically visualized and typed by exposing organisms to type-specific antisera that combine with their unique capsular polysaccharide, rendering the capsule refractile (Quellung reaction). Specific antibodies to capsular polysaccharides confer protection on the host, promoting opsonization and phagocytosis. Additionally, CD4 ⁺ T cells have a direct role in antibody-independent immunity to pneumococcal nasopharyngeal colonization. Conjugated PCVs promote T-cell immunity and protect against pneumococcal colonization, in contrast to the pneumococcal polysaccharide vaccine (PPSV23) that is used in adults and certain high-risk pediatric populations and that does not affect nasopharyngeal colonization.

Epidemiology

Most healthy individuals carry various S. pneumoniae serotypes in their upper respiratory tract; >90% of children between 6 mo and 5 yr of age harbor S. pneumoniae in the nasopharynx at some time. A single serotype usually is carried by a given individual for an extended period (45 days to 6 mo). Carriage does not consistently induce local or systemic immunity sufficient to prevent later reacquisition of the same serotype. Rates of pneumococcal carriage peak during the 1st and 2nd yr of life and decline gradually thereafter. Carriage rates are highest in institutional setting and during the winter, and rates are lowest in summer. Nasopharyngeal carriage of pneumococci is common among young children attending out-of-home care, with rates of 21–59% in point prevalence studies.

Before the introduction of heptavalent pneumococcal conjugate vaccine ( PCV7 ) in 2000, serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F caused most invasive childhood pneumococcal infections in the United States. The introduction of PCVs resulted in a marked decrease in invasive pneumococcal infections (IPIs) in children. By 2005, however, IPIs began to increase slightly because of an increase in non-PCV7 serotypes, particularly serotype 19A. Serotype replacement can result from expansion of existing nonvaccine serotypes, as well as from vaccine-type pneumococci acquiring the polysaccharide capsule of a nonvaccine serotype ( serotype switching ). Since the introduction of PCV13 in 2010 in the United States, there has been a decline in IPIs caused by new vaccine serotypes, including 19A. Nonetheless, 19A remains an important cause of meningitis. Indirect protection of unvaccinated persons has occurred since PCV introduction, and this herd protection is likely a result of decreases in nasopharyngeal carriage of virulent pneumococcal vaccine serotypes.

S. pneumoniae is the most frequent cause of bacteremia, bacterial pneumonia, otitis media, and bacterial meningitis in children. The decreased ability in children <2 yr old to produce antibody against the T-cell–independent polysaccharide antigens and the high prevalence of colonization may explain an increased susceptibility to pneumococcal infection and the decreased effectiveness of polysaccharide vaccines. Children at increased risk of pneumococcal infections include those with sickle cell disease, asplenia, deficiencies in humoral (B-cell) and complement-mediated immunity, HIV infection, certain malignancies (e.g., leukemia, lymphoma), chronic heart, lung, or renal disease (particularly nephrotic syndrome), cerebrospinal fluid (CSF) leak, and cochlear implants. Table 209.1 lists other high-risk groups. Some American Indian, Alaska Native, and African American children may also be at increased risk. Children <5 yr old in out-of-home daycare are at increased risk (approximately 2-fold higher) of experiencing IPIs than other children. Males are more frequently affected than females. Because immunocompetent vaccinated children have had fever episodes of IPI, the proportion of infected children with immunologic risk factors has increased (estimated at 20%).

Pneumococcal disease usually occurs sporadically but can be spread from person to person by respiratory droplet transmission. S. pneumoniae is an important cause of secondary bacterial pneumonia in patients with influenza. During influenza epidemics and pandemics, most deaths result from bacterial pneumonia, and pneumococcus is the predominant bacterial pathogen isolated in this setting. Pneumococcal copathogenicity may be important in disease caused by other respiratory viruses as well.