Mechanism of action Hemophilus influenzae type b is encapsulated and thus resistant to phagocytosis by white blood cells. Hemophilus influenzae type b multiplies rapidly in the bloodstream and enters the CSF, inflaming the meninges. The disease progresses very rapidly, and death results from shock and inflammation caused by the release of endotoxins from the bacteria's gram negative cell wall. One component of the outer membrane of the cell wall is the lipopolysaccharides. The endotoxin lipid A is the lipid portion of the lipopolysaccharides.
Shock occurs when blood pressure is lost rapidly.
However, remember that Hemophilus influenzae type b has a capsule that does not allow it to be phagocytized. Invasion in the CSF by Hemophilus influenzae type b may finally lead to functional and structural injury to the brain. Hemophilus influenzae type b causes menigitis mostly in children before age four. Most of the cases occur at about 6 months of age, probably because that is the time when the immunity from antibodies provided by the mother weakens. This is a time of weakened host defenses during which it is easier for Hemophilus influenzae type b to multiply within the bloodstream.