Factor H binding protein is key to the pathogenesis of N. meningitidis, and is, therefore, important as a potential vaccine candidate. Porins are also an important factor for complement inhibition for both pathogenic and commensal species. Porins are important for nutrient acquisition. Porins are also recognized by TLR2, they bind complement factors (C3b, C4b, factor H, and C4bp (complement factor 4b-binding protein)). Cooperation with pili for CR3-mediated internalization is another function of porins. Ability to translocate into host cells and modulate reactive oxygen species production and apoptosis is made possible by porins, as well. Strains of the same species can express different porins. Genome
At least 8 complete genomes of Neisseria meningitidis strains have been determined which encode about 2,100 to 2,500 proteins.The genome of strain MC58 (serogroup B) has 2,272,351-base pairs. When sequenced in 2000, it was found to contain 2158 open reading frames (ORFs). Of these, a biological function was predicted for 1158 (53.7%). There were three major islands of horizontal DNA transfer found. Two encode proteins involved in pathogenicity. The third island only codes for hypothetical proteins. They also found more genes that undergo phase variation than any pathogen then known. Phase variation is a mechanism that helps the pathogen to evade the immune system of the host.The genome size of strain H44/76 is 2.18 Mb, and encodes 2,480 open reading frames (ORFs), compared to 2.27 Mb and 2,465 ORFs for MC58. Both strains have a GC content of 51.5%.
Other severe complications include Waterhouse–Friderichsen syndrome, a massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia, adrenal insufficiency, and disseminated intravascular coagulation.Not all instances of a purpura-like rash are due to meningococcal septicaemia; other possible causes, such as idiopathic thrombocytopenic purpura (ITP; a platelet disorder) and Henoch–Schönlein purpura, also need prompt investigation. Microbiology
N. meningitidis is a Gram-negative diplococcus since it has an outer and inner membranes with a thin layer of peptidoglycan in between. It is 0.6–1.0 micrometers in size. It tests positive for the enzyme cytochrome c oxidase. Habitat
N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 8–25% of adults. It colonizes and infects only humans, and has never been isolated from other animals. This is thought to result from the bacteriums inability to get iron from sources other than human transferrin and lactoferrin. Subtypes
Disease-causing strains are classified according to the antigenic structure of their polysaccharide capsule. Serotype distribution varies markedly around the world. Among the 13 identified capsular types of N. meningitidis, six (A, B, C, W135, X, and Y) account for most disease cases worldwide. Type A has been the most prevalent in Africa and Asia, but is rare/practically absent in North America. In the United States, serogroup B is the predominant cause of disease and mortality, followed by serogroup C. The multiple subtypes have hindered development of a universal vaccine for meningococcal disease. Pathogenesis
Virulence
Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis.