Still a serious disease: Despite advances in antibiotic therapy, and despit
e the emergence of beta-lactam-resistant strains, mortality of pneumococcal
pneumonia has remained relatively unchanged. The pathogenicity of a pneumo
coccal strain results from an interaction between a specific host with its
own capacity to "resist or yield" to the multiple virulence factors intrins
ic to each S. pneumoniae strain.
Role of the capsule: The capsule is the pneumococci's principal arm of resi
stance against the host's defense systems. There is a wide variability depe
nding on the capsule serotype. Inversely, the capsule plays no role in trig
gering the inflammatory reaction which is secondary to substances released
from the bacterial wall such as teichoic acid and peptidoglycan.
Host response: The molecular mechanisms of cellular activation and inductio
n of proinflammatory cytokins triggered by S. pneumoniae follow similar pat
hways which are different from those for endotoxin triggered by Cram negati
ve bacteria.
Perspectives: A better understanding of the clinical expression, distinguis
hing simple nasopharyngeal carriage from bacterial pneumonia should lead to
the design of new therapeutic agents which will reduce the capacity of cer
tain S. pneumoniae strains to invade the host and trigger deleterious infla
mmatory reactions.