Serogroup C accounts for almost 70% of the cases in older children, teens and young adults and is vaccine preventable.  There is currently no vaccine to prevent group B in the US however there are some in the near future.

The natural habitat and reservoir for meningococci is the mucosal surfaces of the human nasopharynx and, to a lesser extent, the urogenital tract and anal canal. Approximately 5-10% of adults are asymptomatic nasopharyngeal carriers, but that number increases to as many as 60-80% of members of closed populations (eg, military recruits in camps, boarding schools, dormitories, crowded living conditions, smoking or living with smokers, youth camps, daycares and the practicing of sharing food, drinks, water bottles, unclean toys,  makeup and cigarettes. Some experts believe bar patronage and  kissing also may increase the risk.).

The modes of infection include direct contact or respiratory droplets from the nose and throat of infected people. Meningococcal disease most likely occurs within a few days of acquisition of a new strain, before the development of specific serum antibodies.

The incubation period averages 3-4 days (range 1-10 days), which is the period of communicability. Bacteria can be found for 2-4 days in the nose and pharynx and for up to 24 hours after starting antibiotics. Treatment with penicillin may not eradicate the bacteria from the nasopharyngeal carriers.

After adherence to the nasopharyngeal mucosa, meningococci are transported to membrane-bound phagocytic vacuoles. Within 24 hours, they can be seen in the submucosa, close to vessels and local immune cells. In most cases, meningococcal colonization of mucosal surfaces leads to subclinical infection or mild symptoms. In approximately 10-20% of cases, N meningitidis enters the bloodstream. In the vascular compartment, they may be killed by bactericidal antibodies, complement, and phagocytic cells or may multiply, initiating the bacteremic phase. Organisms replicate rapidly.

Invasive disease depends on host factors. Infants are protected from meningococcal disease for the first few months of life by transferred maternal antibodies and low rate of meningococcal acquisition. Subsequently, susceptibility peaks at age 6-12 months and decreases again after colonization of closely related nonpathogenic bacteria such as Neisseria lactamica that have surface antigens in common with virulent strains. Colonization with N meningitidis gradually replaces the nonpathogenic bacteria and induces antibodies to the infecting strain, thus reinforcing natural immunity. Invasive disease occurs if no protective bactericidal antibodies are mounted against the infecting strain.

Meningococci that elaborate a capsule can lead to invasive disease. The capsule protects them from desiccation and from host immune mechanisms. Adhesins and endotoxins also enhance their pathogenic potential. Dysfunctional properdin (ie, component of the alternative pathway of complement), HIV infection, functional or anatomical asplenia, and congenital complement deficiencies also predispose individuals to meningococcal disease.

• In the US: Since 1960, the incidence has been stable, at approximately 0.9-1.5 cases per 100,000 people per year. Most cases occur during winter and early spring. In the United States, increased frequency of serogroups B and Y meningococci has been noted since 1990. The frequency of localized outbreaks has increased since 1991.

• Internationally: Serogroups A, B, and C are responsible for most cases of meningococcal disease throughout the world.

  In Europe and the Americas, serogroup B is the predominant agent causing meningococcal disease, followed in frequency by serogroup C. Historically, serogroup A was the main cause of epidemic meningococcal disease globally, and serogroup A is still the predominant cause of meningococcal meningitis in Africa and Asia.

  In the African "meningitis belt" (a region of savanna that extends from Ethiopia in the east to Senegal in the west), this disease frequently occurs in epidemics during the hot and dry weather (December to March).

  The recent meningococcal meningitis pandemic, which began in 1996, has resulted so far in approximately 300,000 cases being reported to the World Health Organization (WHO).

• Even when the disease is diagnosed early and adequate therapy is instituted, the case-fatality rate ranges from 5-10% and may exceed 40% in patients with meningococcal sepsis. In a review of 493 episodes of bacterial meningitis in adults, the overall case-fatality rate was 25%. In another study, patients with meningococcal meningitis had a case-fatality rate of 7.5%.

• In developing countries, the mortality rate from bacterial meningitis is often higher (20-40%) than in developed countries.

• Among those who survive the meningococcal disease, 10-20% experience neurological sequelae.

In one study conducted in the United States, males accounted for 55% of total cases of meningococcal meningitis.

Meningococcal meningitis most commonly affects individuals aged between 3 years and adolescence. It rarely occurs in individuals older than 50 years.