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Neisseriameningitidis is a common commensal bacterium of the human upper respiratory tract. Colonization infrequently leads to disseminated disease, but the resulting meningitis and sepsis can be fulminant and rapidly fatal in healthy children and adults. Among survivors, 11% to 19% are left with disabilities such as neurological deficit, hearing loss, or limb amputation.1,2 Despite advances in vaccine technology, N meningitidis remains a significant worldwide pathogen and the cause of epidemic meningitis. Children and young adults bear the burden of disease.




Humans are the only reservoir for N meningitidis, and approximately 10% of the general population are asymptomatic, nasopharyngeal carriers. Peak colonization rates of 24% to 37% occur in healthy adolescents and young adults.4 The colonization rate increases even more under conditions of crowdingin which people from diverse regions are brought together, such as with military recruits, pilgrims, and prisoners, or during outbreaks and epidemics. The majority of these strains are not pathogenic, but carriage often results in protective, serum antibodies.1-5 Even colonization with a virulent clone infrequently leads to disease, but when dissemination occurs, it is often in the first week after acquisition.2,6 Serum bactericidal antibody that activates complement has been shown to be responsible for blocking the dissemination of meningococci from the nasopharynx.7,8 Baseline endemic disease can be punctuated with localized outbreaks or epidemics caused by virulent, genetically related (focal complex) strains.2


In the United States, the rate of meningococcal disease remained relatively stable at 0.9 to 1.5 cases per year per 100,000 population between 1960 and 1999, or 2500 to 3000 cases per year.1 The rate of disease then declined yearly until 2004 and has remained steady through 2006 at 0.3 cases per 100,000 population.9 The prevalence of serum bactericidal antibody is lowest in infants 6 to 24 months of age, and this window of susceptibility correlates with the peak incidence of meningococcal disease.10 Rates drop during childhood, and then a second, smaller peak occurs during adolescence and early adulthood.1,9 The prevalence of meningococcal disease varies seasonally, with the highest attack rates occurring in the winter and early spring.


In the 1980s and early 1990s, most of the disease in the United States was due to serogroups B and C. Recently, group Y increased in prevalence and now accounts for about one third of the cases. Serogroup A is rarely found.1,9 Epidemics have not occurred in the United States since World War II, but Rosenstein et al1,11 reported that beginning in 1991, the frequency of focal outbreaks has increased and is caused by groups of closely related strains, predominantly serogroups C and Y. While these outbreaks generate anxiety and media attention, they account for only 2% to 3% of the yearly disease.1


A multicenter surveillance study of invasive meningococcal disease in ...

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