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