Purpose of review
Infection with Streptococcus pneumoniae (pneumococcus) results in colonization, which can lead to local or invasive disease, of which pneumonia is the most common manifestation. Despite the availability of pneumococcal vaccines, pneumococcal pneumonia is the leading cause of community and inhospital pneumonia in the United States and globally. This article discusses new insights into the pathogenesis of pneumococcal disease.
The host–microbe interactions that determine whether pneumococcal colonization will result in clearance or invasive disease are highly complex. This article focuses on new information in three areas that bear on the pathogenesis of pneumococcal disease: factors that govern colonization, the prelude to invasive disease, including effects on colonization and invasion of capsular serotype, pneumolysin, surface proteins that regulate complement deposition, biofilm formation and agglutination; the effect of coinfection with other bacteria and viruses on pneumococcal growth and virulence, including the synergistic effect of influenza virus; and the contribution of the host inflammatory response to the pathogenesis of pneumococcal pneumonia, including the effects of pattern recognition molecules, cells that enhance and modulate inflammation, and therapies that modulate inflammation, such as statins.
Recent research on pneumococcal pathogenesis reveals new mechanisms by which microbial factors govern the ability of pneumococcus to progress from the state of colonization to disease and host inflammatory responses contribute to the development of pneumonia. These mechanisms suggest that therapies which modulate the inflammatory response could hold promise for ameliorating damage stemming from the host inflammatory response in pneumococcal disease.