Meningococcal disease

Meningococcal disease occurs worldwide as isolated (sporadic) cases, institution- or community-based outbreaks, and large epidemics.

A meningococcus that enters the blood from the nasopharynx and survives host defenses generally has one of two fates. If multiplication occurs slowly, the bacteria eventually seed local sites, such as the meninges, joints, or pericardium. More rapid multiplication in the blood is associated with disseminated intravascular coagulation (DIC) and shock, which usually cause symptoms before local sites become infected. There is thus a remarkable compartmentalization of bacterial growth and host inflammation in either the blood or a local site, usually the meninges.

Patients who develop meningitis may be individuals in whom meningococci do not grow rapidly in the blood; they may have a more vigorous initial inflammatory response to invading meningococci, may have antibodies or phagocytes that slow meningococcal growth, or may lack the (unknown) factors that allow N. meningitidis to multiply rapidly in vivo. The prognosis of patients with meningococcal meningitis is substantially better than that of patients with fulminant meningococcemia

Patients with meningococcal meningitis may develop cranial nerve palsies, cortical venous thrombophlebitis, and cerebral edema. In children subdural effusions may occur. Permanent sequelae can include mental retardation, deafness, and hemiparesis. The major long-term morbidity of fulminant meningococcemia is the loss of skin, limbs, or digits that results from ischemic necrosis and infarction.

There is currently no vaccine for serogroup B; its polysaccharide is a sialic acid homopolymer that is poorly immunogenic in humans. In addition to individuals with late-complement-component or properdin deficiency, persons with sickle cell anemia, asplenia, or splenectomy should receive the quadrivalent vaccine.