Neisseria meningitidis is the bacteria that causes meningitis, a severe infection of the meninges—the thin lining covering the brain and spinal cord. Meningitis can lead to severe illness and, if not treated promptly, can be fatal. Neisseria meningitidis is also known as meningococcus.
Symptoms of meningococcal infection can include fever, headache, stiff neck, and a characteristic rash. The disease can progress rapidly, so prompt medical attention is crucial.
Meningococcal outbreaks can occur in crowded or communal living settings like college campuses or military barracks.
Table of Contents
Capsular polysaccharides
Neisseria meningitidis strains are frequently encapsulated and 13 different capsular serogroups have been found so far. These capsular polysaccharides protect the meningococci from the action of phagocytic cells and enhance organism’s survival during the bloodstream and central nervous system invasion.
Meningococcal capsular polysaccharides do not mediate adherence to epithelial cells, and encapsulated cells adhere to mucosal cells less readily than nonencapsulated cells.
IgA1 protease
All meningococci produce IgA1 protease which serves as a virulence factor by abrogating mucosal immunity. During meningococcal disease and also in asymptomatic nasopharyngeal carriage state, antibodies against IgA1 protease are produced and are detectable.
Plasmids
Although Neisseria meningitidis have been found containing tetracycline-resistant plasmids, plasmids are not common in Neisseria meningitidis. Meningococci containing beta-lactamase gene has been found and plasmid it carries is virtually identical with those of Neisseria gonorrhoeae.
Fimbriae (Pili)
Neisseria meningitidis is a piliated organism; the pili mediate attachment of the organism to the mucosal cells of the nasopharynx. It is still not known, whether the pili play a role in the ability of meningococci to cross the blood-brain barrier or to interact with meningeal tissues.
Lipooligosaccharides
Neisseria meningitids contains lipooligosaccharides, that lacks the repeating O antigens. Lipooligosaccharide has carbohydrate lacto-N-neotetrose, which is one of the established meningococcal virulence determinants. Meningococcal lipooligosaccharide also stimulates the release of TNF-alpha, which results in host cell damage.
PorA and PorB proteins
These are the outer-membrane proteins of Neisseria meningitidis. It has been proved that porB proteins can insert themselves into the membrane of target cells and phagolysosomes and induce apoptosis, thereby facilitating infection and invasion of the host.
Opa and Opc proteins
These proteins facilitate bacterial adherence to epithelial cells and neutrophils. Types of opa proteins expressed differ between isolates of different anatomic sites. Opc proteins functions in mucosal adherence and invasion of endothelial cells. Opc protein is also a target of bactericidal antibodies.
Iron-Binding/Acquisition proteins
These are the integral membrane proteins of Neisseria meningitidis. They help in the acquisition of iron from human transferrin, lactoferrin, and hemoglobin/haptoglobin.
References
- Rouphael, N. G., & Stephens, D. S. (2012). Neisseria meningitidis: biology, microbiology, and epidemiology. Methods in molecular biology (Clifton, N.J.), 799, 1–20. https://doi.org/10.1007/978-1-61779-346-2_1
- Unkmeir, A., Kämmerer, U., Stade, A., Hübner, C., Haller, S., Kolb-Mäurer, A., Frosch, M., & Dietrich, G. (2002a). Lipooligosaccharide and polysaccharide capsule: Virulence factors ofneisseria meningitidisthat determine meningococcal interaction with human dendritic cells. Infection and Immunity, 70(5), 2454–2462. https://doi.org/10.1128/iai.70.5.2454-2462.2002
