The first definitive recognition of epidemic meningitis in the United States occurred in Medfield, Massachusetts, in 1806, 1 year after its first description in Geneva ( 73, 74, 367). More extensive general reviews of the clinical manifestations and therapy of meningococcal disease and bacterial meningitis can be found elsewhere ( 10, 354, 355). The purpose of this paper is to review these developments. In recent years, there have been changes in the epidemiology of meningococcal disease and new opportunities for vaccine prevention. A striking feature of the meningococcus is that much of its genetic variability is achieved through genetic recombination, which gives the organism the ability to rapidly acquire new traits in response to selective pressures ( 100, 101, 190, 357).
It most commonly causes asymptomatic nasopharyngeal carriage but on occasion causes invasive disease ( 10, 58, 150). meningitidis is a gram-negative diplococcus that is a strict human pathogen. monocytogenes, and group B streptococcus because of the use of intrapartum chemoprophylaxis in selected women ( 3, 312, 341, 384). The role of the meningococcus as a cause of bacterial meningitis has become more pronounced in recent years with the declines in meningitis caused by Haemophilus influenzae type b and Streptococcus pneumoniae because of the introduction of new conjugate vaccines, Listeria because of efforts to reduce the contamination of food with L. Neisseria meningitidis is a leading cause of bacterial meningitis and other invasive bacterial infections, both in the United States and worldwide ( 244, 300, 314).
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