The PNEUMONIA Times
Recent concepts in host-microbe interaction leading to pneumococcal pneumonia
Infection with Streptococcus pneumoniae can lead to either a local or invasive disease, having pneumonia as one of the most common manifestations. Despite having pneumococcal vaccines, pneumococcal pneumonia is still the leading cause of community and in-hospital pneumonia in the world.
Streptococcus pneumoniae is an encapsulated Gram-positive microbe that colonizes the human nasopharynx. The virulence factor of pneumococcus is a polysaccharide capsule (CPS) that provides the bacterium with a mechanism of antigen variation and confers serotype specificity. Patients can be infected from asymptomatic nasopharyngeal colonization to local (otitis media) and distant invasive pneumococcal disease (IPD), including meningitis, pneumonia and bacteremia (bloodstream invasion). Pneumococcus is one of the most common and lethal cause of outpatient and inpatient pneumonias, which are associated with substantial morbidity, mortality and rising health care costs, particularly in the elderly.
The capsular polysaccharide gives streptococcus pneumoniae its virulence. A new study found that the longer pneumococcal chain length, the better it facilitates adhesion. Another discovery was made that pneumococcal serotypes undergo microevolution due to mutations in the wcjE (O-acetyltransferase) gene, whereby colonizing strains exhibit phenotypic switching and become invasive strains.
Pneumococcal biofilm formation has also been associated with nasopharyngeal colonization. In one study, pneumococcal serine-rich repeat protein (PsrP), a surface protein and lung-specific virulence factor, promoted bacterial aggregation and biofilm structures in the nasopharynx and lungs of mice. Since genetic material is exchanged among co-colonizing strains of pneumococcus during biofilm growth, the phenotype of one strain could be affected.
New insights into regulation of the pneumococcal biofilm phenotype have begun to emerge. Binding of an agglutinating CPS-specific monoclonal antibody did enhance pneumococcal quorum sensing. These antibodies did not induce phagocyte-mediated bacterial killing in vitro although they were protective in mice, suggesting that antibody-mediated agglutination did not kill pneumococcal growth. Thus, antibody agglutination of pneumococcus does not necessarily benefit the host as the antibodies seen in mice did not induce bacterial clearance.
Other microbes found in the nasopharynx can also influence pneumococcal colonization and invasiveness. Some studies have shown that pneumococcal adherence was inhibited by bacteriocins produced by S. mitis and S. salivarius from healthy children. In one study, virulent pneumococcal serotypes emerged during nasopharyngeal competition with Haemophilus influenzae. However, in another, pneumococcal colonization correlated negatively with α-hemolytic streptococci during asymptomatic viral upper respiratory infection (URI), but in viral URI with otitis media, pneumococcal and non-typeable Haemophilus influenzae colonization each increased while α-hemolytic streptococci decreased.
References:
- Vernatter, J, Pirofski, P (2014). Current concepts in host-microbe interaction leading to pneumococcal pneumonia. Pubmed. Retrieved 2nd December 2015, from <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237063/>