Infection with Neisseria meningitidis most commonly manifests as asymptomatic colonization in the nasopharynx of healthy adolescents and adults. Invasive disease occurs rarely, usually presenting as either bacterial meningitis or meningococcal septicemia. Patients may also present with occult bacteremia, pneumonia, septic arthritis, conjunctivitis, and chronic meningococcemia.
Etiology and Microbiology
N. meningitidis is a gram-negative aerobic diplococcus that colonizes humans only and that causes disease after transmission to a susceptible individual. Several related organisms have been recognized, including the pathogen N. gonorrhoeae and the commensals N. lactamica, N. flavescens, N. mucosa, N. sicca, and N. subflava . N. meningitidis is a catalase- and oxidase-positive organism that utilizes glucose and maltose to produce acid.
Meningococci associated with invasive disease are usually encapsulated with polysaccharide, and the antigenic nature of the capsule determines an organism's serogroup (Table 143-1). In total, 13 serogroups have been identified (A–D, X–Z, 29E, W135, H–J, and L), but just 5 serogroups—A, B, C, Y, and W135—account for the majority of cases of invasive disease. Acapsular meningococci are commonly isolated from the nasopharynx in studies of carriage; the lack of capsule often is a result of phase variation of capsule expression, but as many as 16% of isolates lack the genes for capsule synthesis and assembly. These “capsule-null” meningococci and those that express capsules other than A, B, C, Y, and W135 are only rarely associated with invasive disease and are most commonly identified in the nasopharynx of asymptomatic carriers.
Table 143-1 Structure of the Polysaccharide Capsule of Common Disease-Causing Meningococci |Favorite Table|Download (.pdf)
Table 143-1 Structure of the Polysaccharide Capsule of Common Disease-Causing Meningococci
|Meningococcal Serogroup||Chemical Structure of Oligosaccharide||Current Disease Epidemiology|
|A||2-Acetamido-2-deoxy-D-mannopyranosyl phosphate||Epidemic disease mainly in sub-Saharan Africa; sporadic cases worldwide|
|B||α-2,8-N-acetylneuraminic acid||Sporadic cases worldwide; propensity to cause hyperendemic disease|
|C||α-2,9-O-acetylneuraminic acid||Small outbreaks and sporadic disease|
|Y||4-O-α-D-glucopyranosyl-N-acetylneuraminic acid||Sporadic disease and occasional small institutional outbreaks|
|W135||4-O-α-D-galactopyranosyl-N-acetylneuraminic acid||Sporadic disease; outbreaks of disease associated with mass gatherings; epidemics in sub-Saharan Africa|
Beneath the capsule, meningococci are surrounded by an outer phospholipid membrane containing lipopolysaccharide (LPS, endotoxin) and multiple outer-membrane proteins (Figs. 143-1 and 143-2). Antigenic variability in porins expressed in the outer membrane defines the serotype (PorB) and serosubtype (PorA) of the organism, and structural differences in LPS determine the immunotype. Serologic methods for typing of meningococci are restricted by the limited availability of serologic reagents that can distinguish among the organisms′ highly variable surface proteins. Where available, high-throughput antigen gene sequencing has superseded serology for meningococcal typing. A large database of antigen gene sequences for the outer-membrane proteins PorA, PorB, FetA, Opa, and factor H–binding protein is available online (www.neisseria.org). The number of specialized iron-regulated ...