Abstract
Defining the propensity of Streptococcus pneumoniae (SP) serotypes to invade sterile body sites following nasopharyngeal (NP) acquisition has the potential to inform about how much invasive pneumococcal disease (IPD) may occur in a typical population with a given distribution of carriage serotypes. Data from enhanced surveillance for IPD in Massachusetts children ≤7 years in 2003/04, 2006/07 and 2008/09 seasons and surveillance of SP NP carriage during the corresponding respiratory seasons in 16 Massachusetts communities in 2003/04 and 8 of the 16 communities in both 2006/07 and 2008/09 were used to compute a serotype specific “invasive capacity (IC)” by dividing the incidence of IPD due to serotype x by the carriage prevalence of that same serotype in children of the same age. A total of 206 IPD and 806 NP isolates of SP were collected during the study period. An approximate 50-fold variation in the point estimates between the serotypes having the highest (18C, 33F, 7F, 19A, 3 and 22F) and lowest (6C, 23A, 35F, 11A, 35B, 19F, 15A, and 15BC) IC was observed. Point estimates of IC for most of the common serotypes currently colonizing children in Massachusetts were low and likely explain the continued reduction in IPD from the pre-PCV era in the absence of specific protection against these serotypes. Invasive capacity differs among serotypes and as new pneumococcal conjugate vaccines are introduced, ongoing surveillance will be essential to monitor whether serotypes with high invasive capacity emerge (e.g. 33F, 22F) as successful colonizers resulting in increased IPD incidence due to replacement serotypes.
Highlights
The pathogenesis of invasive pneumococcal disease (IPD) begins with nasopharyngeal (NP) colonization that proceeds, often through local infection, to blood stream invasion
Serotype distribution A total of 206 isolates of S. pneumoniae causing invasive disease in children
The proportion of isolates included in PCV7 was 16.9% in the 2004 respiratory season, whereas only one (1.1%) of the IPD cases in the 2009 season was due to a vaccine serotype
Summary
The pathogenesis of invasive pneumococcal disease (IPD) begins with nasopharyngeal (NP) colonization that proceeds, often through local infection, to blood stream invasion. Differences in invasive capacity of more than 90 known capsular serotypes have been assumed to depend primarily on the antiphagocytic properties of the capsular polysaccharides rather than surface proteins, it is likely that each contributes to the capacity of specific strains to produce blood stream invasion or mucosal surface infection [4]. Support for this concept is derived from the observation that isolates lacking a capsule are rarely detected as a cause of invasive disease in patients or animal models [4,5,6]. Investigating the propensity for a specific serotype to invade sterile body sites once NP acquisition occurs can suggest how much IPD we may anticipate in a population with any particular distribution of serotypes in carriage
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