The risk of meningococcal disease is higher among asplenic individuals and those with deficiencies in the terminal common complement pathway of the immune system (CDC, 2005). Additionally, prior viral infection, crowding, active and passive smoking, attending bars or nightclubs, and imbibing in alcohol are all associated with higher risk of meningococcal disease (CDC, 2005).
Prior to the development of antibiotics, approximately 70 to 85 percent of cases of meningococcal disease were fatal (Granoff et al., 2008). With the introduction of antibiotics, the case-fatality rate has dropped to nearly 30 percent worldwide and 10–14 percent in the United States (CDC, 2005; Granoff et al., 2008). Ten to 20 percent of meningococcal disease survivors experience permanent sequelae such as limb loss, hearing loss, neurologic disability, and scarring (Granoff et al., 2008).
Meningococcus has been grouped into at least 13 different groups based on serological differences in the surface polysaccharides (Apicella, 2010). Of these, five serogroups—A, B, C, W-135, and Y—are responsible for almost all instances of meningococcal disease (Granoff et al., 2008). Group A meningococcus produces the majority of disease in the “ meningitis belt” of sub-Saharan Africa but causes less than 0.3 percent of cases in the United States and Europe (Granoff et al., 2008). Serogroup W-135 was known to cause rare disease until demonstration of W-135 meningococcus in outbreaks in 2000 and 2001 during the Hajj in Mecca, Saudi Arabia (Granoff et al., 2008). In the United States, the majority of meningococcal disease is caused by serogroups B, C, and Y (Granoff et al., 2008). Serogroup B causes more than 50 percent of disease in infants less than 1 year old, and 75 percent of disease in individuals greater than 11 years is caused by serogroups C, Y, or W-135 (CDC, 2005).
Although various vaccines against meningococcal disease have been available for more than 30 years, currently there is no vaccine to protect against all five of the pathogenic serogroups. During the early 1900s, attempts were made to develop inactivated whole-cell vaccine, but this direction was abandoned due to ambiguous efficacy results and high rates of reactogenicity (Gates, 1918; Granoff et al., 2008; Sophian and Black, 1912; Underwood, 1940). The immunogenicity of exotoxin-containing culture filtrates was explored in the 1930s (Ferry and Steele, 1935; Kuhns et al., 1938). The development of antibiotics provided a more effective means to combat meningococcal infection. During the 1940s, it was demonstrated that inoculation with group-specific polysaccharides produced immunogenicity in mice (Scherp and Rake, 1945), but similar inoculation failed to produce the results in humans (Kabat et al., 1944; Watson and Scherp, 1958). It was later determined that the polysaccharide antigens capable of causing immunogenicity in humans were of a higher molecular weight than those used by Scherp and Rake (Gotschlich et al., 1972; Kabat and