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Prevention of invasive meningococcal disease in the United States.

In 2007, the Centers for Disease Control and Prevention estimates that 1000 cases of invasive meningococcal disease (IMD) occurred in the United States, with 130 (13%) case fatalities and an equal rate of morbidity, including primarily amputations and hearing loss. Seventy percent were caused by vaccine preventable serogroups (C, Y and W135). In the next 2 years, it is likely that meningococcal conjugate vaccines (A, C, Y, and W135; or C and Y) will be licensed for use beginning in infancy. This review will address strategies for, and barriers to, the prevention of IMD caused by vaccine preventable serogroups. Young infants represent the age group most vulnerable to IMD. The incidence of disease in children less than 1 year of age averaged 8.5 cases per 100,000 between 1997 and 2002; this is 2.5-fold greater than in children between 1 and 2 years of age, and at least 5-fold greater than adolescents age 14–24 years. In 2007, the total number of cases of IMD in the United States was the lowest in more than 4 decades ( 1000), yet the incidence among children less than 1 year of age (2.8/100,000) was still greater than any other age group (10-fold the rate in 11–17 year olds and 2.8 times the rate in young adults 18–22 years). One hundred and thirty individuals succumbed to IMD in 2007, and an equal number suffered serious morbidity; approximately 15 of these deaths were in children age less than 1 year. Morbidity and mortality from IMD have each persisted at approximately 10% in the United States for the past decade, with a lower rate in children and a higher rate in adolescents and young adults. The challenge continues to be early identification, because many of those who succumb present with disseminated intravascular coagulation, and new interventions (such as activated protein C), have not improved the outcome of septic shock in children. Strategies for prevention of meningococcal disease require an understanding of the transmission of Neisseria meningitidis and pathogenesis of disease to improve approaches for reducing disease burden and mortality. Two principles require consideration in development of approaches to immunoprophylaxis. First, unlike pneumococcal and Haemophilus influenzae type b (Hib) diseases, which primarily colonize toddlers, carriage rates of encapsulated N. meningitidis are low in the first year of life, increase in teenagers, and peak at 20 to 24 years of age. This observation suggests that adolescents and young adults are the source of transmission to the community, although spread from toddler to toddler is not uncommon in settings such as day care. The second principle is that recent acquisition is primarily associated with development of disease in susceptible individuals, and that serum bactericidal antibody (BCA) is protective. Goldschneider, et al observed that BCA was highest at birth and among adults, and lowest among children age 6 to 24 months. Sera from more than 90% of prospective cases in military recruits were deficient in antibodies. Furthermore, recent re-emergence of Hib disease in the United Kingdom suggests that induction of immune memory without durable concentrations of serum antibody was insufficient for protection. In further support of the concept that circulating antibody is needed for protection, 3 infant doses of meningococcal C conjugate (MCC) vaccine elicited immunologic memory and initially demonstrated protection against IMD, which decayed substantially in year 2 of life. Protection against IMD will require eliciting durable serum antibody present at the time of acquisition of N. meningitidis, and sufficient antibody to decrease colonization in adolescents and young adults, if the goal of population-based reduction in disease is to be achieved.