Neisseria meningitidis, often referred to as the meningococcus, is a Gram-negative bacterium that can cause meningitis and other forms of meningococcal disease such as meningococcemia, a life-threatening sepsis.

[2] N. meningitidis is spread through saliva and respiratory secretions during coughing, sneezing, kissing, chewing on toys and through sharing a source of fresh water.

[3] It infects its host cells by sticking to them with long thin extensions called pili and the surface-exposed proteins Opa and Opc and has several virulence factors.

[4] It initially produces general symptoms like fatigue, fever, and headache and can rapidly progress to neck stiffness, coma and death in 10% of cases.

[5] Symptoms of meningococcal meningitis are easily confused with those caused by other bacteria, such as Haemophilus influenzae and Streptococcus pneumoniae.

Current guidance in the United Kingdom is that if a case of meningococcal meningitis or septicaemia (infection of the blood) is suspected, intravenous antibiotics should be given and the ill person admitted to the hospital.

[8] This means that laboratory tests may be less likely to confirm the presence of Neisseria meningitidis as the antibiotics will dramatically lower the number of bacteria in the body.

[7] Factor H binding protein (fHbp) that is exhibited in N. meningitidis and some commensal species is the main inhibitor of the alternative complement pathway.

Ability to translocate into host cells and modulate reactive oxygen species production and apoptosis is made possible by porins, as well.

[19] The complete genome sequence of strain NMA510612 (serogroup A) consists of one circular chromosome with a size of 2,188,020 bp, and the average GC content is 51.5%.

[24] Consequently, an important benefit of genetic transformation to N. meningitidis may be the maintenance of the recombination and repair machinery of the cell that removes oxidative DNA damages such as those caused by reactive oxygen.

This is consistent with the more general idea that transformation benefits bacterial pathogens by facilitating repair of DNA damages produced by the oxidative defenses of the host during infection.

[17] The commensal species of Neisseria can act as a reservoir of genes that can be acquired; for example, this is how capsule switching can occur as a means of hiding from the immune system.

The diagnosis is suspected, when Gram-negative diplococci are seen on Gram stain of a centrifuged sample of CSF; sometimes they are located inside white blood cells.

[4] The gold standard of diagnosis is microbiological isolation of N. meningitidis by growth from a sterile body fluid, which could be CSF or blood.

Gram negative diplococci that are oxidase and catalase positive are then tested for fermentation of the following carbohydrates: maltose, sucrose, and glucose.

Finally, serology determines the subgroup of the N. meningitidis, which is important for epidemiological surveillance purposes; this may often only be done in specialized laboratories.

[citation needed] The above tests take a minimum of 48–72 hours turnaround time for growing the organism, and up to a week more for serotyping.

This especially includes young children and their child caregivers or nursery-school contacts, as well as anyone who had direct exposure to the patient through kissing, sharing utensils, or medical interventions such as mouth-to-mouth resuscitation.

[29] The Centers for Disease Control and Prevention (CDC) recommends all teenagers receive MenACWY vaccine and booster, with optional MenB.

The vaccine, Menhibrix, was designed to prevent disease caused by Neisseria meningitidis serogroups C and Y, and Haemophilus influenzae type b (Hib).

Beginning in Burkina Faso in 2010, it has been given to 215 million people across Benin, Cameroon, Chad, Ivory Coast, Ethiopia, Ghana, Mali, Niger, Mauritania, Nigeria, Senegal, Sudan, Togo and Gambia.

[34] Clinical practice guidelines endorse empirical treatment in the event a lumbar puncture to collect cerebrospinal fluid (CSF) for laboratory testing cannot first be performed.

[34][35] Antibiotic treatment may affect the results of microbiology tests, but a diagnosis may be made on the basis of blood-cultures and clinical examination.

[36] N. meningitidis is a major cause of illness, developmental impairment and death during childhood in industrialized countries and has been responsible for epidemics in Africa and in Asia.

[7] The incidence of meningococcal disease is highest among infants (children younger than one year old) whose immune system is relatively immature.

In industrialized countries there is a second peak of incidence in young adults, who are congregating closely, living in dormitories or smoking.

Other risk factors include a weakened general or local immune response, such as a recent upper respiratory infection, smoking, and complement deficiency.

In susceptible individuals, N. meningitidis may invade the bloodstream and cause a systemic infection, sepsis, disseminated intravascular coagulation, breakdown of circulation, and septic shock.

[citation needed] In 1884 Ettore Marchiafava and Angelo Celli first observed the bacterium inside cells in the cerebral spinal fluid (CSF).