N meningitidis causes both endemic and epidemic disease, principally meningitis and meningococcemia. As a result of the control of Haemophilus influenzae type b infections, N meningitidis has become the leading cause of bacterial meningitis in children and young adults in the United States (US), with an estimated 2,600 cases each year.^5,6 The case-fatality rate is 13% for meningitis disease (defined as the isolation of N meningitidis from cerebrospinal fluid) and 11.5% for persons who have N meningitidis isolatedfrom blood,^5,6 despite therapy with antimicrobial agents (eg, penicillin) to which US strains remain clinically sensitive.⁵

The incidence of meningococcal disease peaks in late winter to early spring. Based on multistate surveillance conducted during 1989 to 1991, serogroup B organisms accounted for 46% of all cases and serogroup C for 45%; serogroups W-135 and Y and strains that could not be serotyped accounted for most of the remaining cases.^5,6 Recent data indicate that the proportion ofcases caused by serogroup Y strains is increasing.⁵ In 1995, among the 30 states reporting supplemental data on culture-confirmed cases of meningococcal disease, serogroup Y accounted for 21% of cases.⁷ Because of the success of H influenzae type b vaccinations, the median age of persons with bacterial meningitis increased from 15 months in 1986 to 25 years in 1995.⁸ The predominate organism causing meningitis in children 2 to 18 years of age is N meningitidis based on 1995 surveillance data.⁸ Serogroup A, which rarely causes disease in the US, is the most common cause of epidemics in Africa and Asia. A statewide serogroup B epidemic has been reported in the US.⁹ Within the US, a vaccine for serogroup B is not yet available.

Outbreaks of serogroup C meningococcal disease (SCMD) have been occurring more frequently in the US since the early 1990s, and the use of vaccine to control these outbreaks has increased.⁵ During 1980-1993, 21 outbreaks of SCMD were identified; eight of these occurred during 1992-1993.¹⁰ Each of these 21 outbreaks involved from three to 45 cases of SCMD, and most outbreaks had attack rates exceeding 10 cases per 100,000 population, which is approximately 20 times higher than rates of endemic SCMD.⁵ During 1981-1988, only 7,600 doses of meningococcal vaccine were used to control four outbreaks; whereas, from January 1992 through June 1993, 180,000 doses ofvaccine were used in response to eight outbreaks.⁵

Several discoveries impacted the future of meningococcal polysaccharide vaccines and demonstrated the significance of anti-capsular antibodies in protection.¹¹ In the late 1930s, serogroup-specific antigens of meningococcal serogroups A and C were identified as polysaccharides.⁹ During the mid 1940s, investigators demonstrated that the protection of mice by anti-serogroup A meningococcal horse serum was directly related to its content of anti-polysaccharide antibodies.¹¹ Meningococcal polysaccharide vaccines were first demonstrated to be immunogenic in humans by Gotschlich and his co-workers in the 1960s when immunization of US Army recruits with serogroup A and C polysaccharides induced protective antibodies.¹¹ The investigators recorded a significantly reduced acquisition rate of serogroup C carriage among vaccinated recruits compared with unvaccinated individuals.¹¹

Persons who have certain medical conditions are at increased risk for developing meningococcal infection. Meningococcal disease is particularly common among persons who have component deficiencies in the terminal common complement pathway (C3, C5-C9); many of these persons experience multiple episodes of infection.⁵Asplenic persons also may be at increased risk for acquiring meningococcal disease with particularly severe infections.⁵ Persons who have other diseases associated with immunosuppression (eg, human immunodeficiency virus [HIV] and Streptococcus pneumoniae) may be at higher risk for developing meningococcal disease and for disease caused by some other encapsulated bacteria.⁵ Evidence suggests that HIV-infected persons are not at substantially increased risk for epidemic serogroup A meningococcal disease;⁵ however, such patients may be at increased risk for sporadic meningococcal disease or disease caused by other meningococcal serogroups.⁵ Previously, military recruits had high rates of meningococcal disease, particularly serogroup C disease; however, since the initiation of routine vaccination of recruits with bivalent A/C meningococcal vaccine in 1971, the high rates of meningococcal disease caused by those serogroups have decreased substantially and cases occur infrequently.⁵

Bookmark this page: