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Evasion of Immune System Detection

One very interesting proposed way in which N. meningitidis evades detection by the body's immune system, involves its ability to regulate production of its antiphagocytic polysaccharide capsule. Researchers such as Hammerschmidt have argued that by losing its capsule, N. meningitidis increases its camoflauge-capabilities, allowing it to colonize the nasopharynx undetected (Hammerschmidt et al., 1996). Another aspect that allows the bacterium in its efforts to evade the immune system is its ability to ulilize gene switching and express phase-variable proteins on its surface, such as PorA and PorB (Yazdankhak et al., 2004); N. meningitidis normally uses these actions in response to changing environmental conditions, but a result is the ability to create genetic diversity.

N. meningitidis produces a number of adhesins, which allow it to rather successfully colonize the nasopharynx with ease. An example of such a molecule is an extracellular IgA1 protease that cleaves human IgA1, which has the essntial role of preventing adherence of bacteria to mucosal tissue (Yazdankhak et al., 2004). By destroying the IgA1, the bacterium has a significantly greater ability to remain in the nasopharynx. As one researcher noted, "the presence of high concentrations of circulating IgA antibodies to N. meningitidis may paradoxically permit the development or exacerbate the progression of invasive disease by preferentially binding to the organism, thereby blocking the beneficial effects of IgG and IgM antibodies" (Tunkel et al.,1993). Additionally, the bacteria has receptors capable of binding to transferrin and lactoferrin, which provide N. meningitidis with the essential iron it needs to grow (Yazdankhak et al., 2004). Research has demonstrated that N. meningitidis begins its infection by latching on to the host cells via type IV pili, which are surface-associated filaments extending from the bacterial surface; CD46, which is a membrane cofactor protein expressed on the vast majority of human cells, happens to be a receptor for the pili (Yazdankhak et al., 2004).

In the vast majority of cases, the N. meningitidis does not evade the immune system and is subsequently destroyed bactericidal antibodies, complement, and phagocytic cells; however, in roughly 10-20% of all infections the bacterium enters the bloodstream and undergoes rapid bacteremia (Gondim et al., 2007). At this point, metastatic meningeal infection or severe systemic infection with circulatory collapse and disseminated intravascular coagulation (DIC) occur within a couple of days (Gondim et al., 2007).

Regardless, it is by far the make-up of the organism's capsule which allows it to perform the vast number of functions it does in order to evade and prevent an immunological response. N. meningitidis's encapsulation contributes to the infectiousness by inhibiting neutrophil phagocytosis and classic complement-mediated bactericidal activity; in turn this enhances bloodstream-survival capabilities of the organism and allows for more effective intravascular replication (Tunkel et al.,1993).




Gondim, F., et al. "Meningococcal Meningitis." EMedicine, from WebMD. (2007) <> Accessed 04/08/07.

Hammerschmidt, S., et al. "Capsule phase variation in Neisseria meningitidis serogroup B by slipped-strand mispairing in the polysialyltransferase gene (siaD): correlation with bacterial invasion and the outbreak of meningococcal disease." Molecular Microbiology 20 (1996): 1211–20.

Tunkel, A.R., and W. Michael Scheld. "Pathogenesis and Pathophysiology of Bacterial Meningitis." Clinical Microbiology Reviews (1993): 118-136.

Yazdankhak, Siamak P., and Dominique A. Caugant. "Neisseria meningitidis: an overview of the carrier stage." Journal of Medical Microbiology 53 (2004): 821-32.



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