Neisseria meningitidis: Biology, Microbiology, and Epidemiology
Neisseria meningitidis (the meningococcus) causes significant morbidity and mortality in children and young adults worldwide through epidemic or sporadic meningitis and/or septicemia. In this review, we describe the biology, microbiology, and epidemiology
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ntroduction In 1887, Weichselbaum (1) was the first to identify the meningococcus from the cerebrospinal fluid (CSF) of a patient with meningitis. Epidemics of meningococcal meningitis were first described during the early nineteenth century, in 1805 in Geneva, Switzerland by Vieusseux (2), in 1806 in New Bedford, Massachusetts by Danielson and Mann (3) and in the early 1900s in the African meningitis belt (4). The meningococcus was recognized as a habitant
Myron Christodoulides (ed.), Neisseria meningitidis: Advanced Methods and Protocols, Methods in Molecular Biology, vol. 799, DOI 10.1007/978-1-61779-346-2_1, © Springer Science+Business Media, LLC 2012
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N.G. Rouphael and D.S. Stephens
of the nasopharynx of healthy individuals (5), especially seen in the setting of military recruits camps (6) at the beginning of the twentieth century. Treatment for meningococcal disease included serum therapy introduced in 1913 by Flexner (7) and sulfonamides introduced in 1937 (8). The emergence of resistance to sulfonamides (9) in the 1960s prompted the development of the first vaccines against meningococci (10). Despite an understanding of the pathogenesis, the availability of therapeutic and prophylactic antibiotics and immunizations against important serogroups, the meningococcus remains a leading cause worldwide of bacterial meningitis (11). Invasive meningococcal disease results from the interplay of: (1) microbial factors influencing the virulence of the organism, (2) environmental conditions facilitating exposure and acquisition, and (3) host susceptibility factors favoring bacterial acquisition, colonization, invasion, and survival. In the pre-serum therapy and pre-antibiotic eras, 70–85% of meningococcal disease cases were fatal; today, the overall mortality rate in invasive meningococcal disease still remains high, at between 10 and 15% (12). Meningococcal disease is also associated with marked morbidity including limb loss, hearing loss, cognitive dysfunction, visual impairment, educational difficulties, developmental delays, motor nerve deficits, seizure disorders, and behavioral problems (13). In this chapter, we review the biology, microbiology, and epidemiology of the meningococcus.
2. Biology of the Meningococcus The virulence (14) of N. meningitidis is influenced by multiple factors: capsule polysaccharide expression, expression of surface adhesive proteins (outer membrane proteins including pili, porins PorA and B, adhesion molecules Opa and Opc), iron sequestration mechanisms, and endotoxin (lipooligosaccharide, LOS). N. meningitidis also has evolved genetic mechanisms resulting in a horizontal genetic exchange, high frequency phase, antigenic variation, and molecular mimicry, allowing the organism to successfully adapt at mucosal surfaces and invade the host (14). 2.1. Genetics
Genome sequences for a number of N. meningitidis strains including MC58 (serogroup B, ST-32) (15), Z2491 (serogroup A, ST-4) (16), FAM18 (serogroup C, ST-11), and NMB-CDC (serogroup B, ST-8) have been reported. Based on the sequencin
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