Epidemiology
In the US, rates of invasive meningococcal infection declined since the late 1990s to a low of 235 (0.07 per 100,000 people) in 2020.[7] Reduced incidence of meningococcal disease has been linked to the introduction of meningococcal conjugate vaccines.[8] However, cases in the US have increased sharply since 2021. In 2024, 503 confirmed and probable cases were reported. This is the largest number of meningococcal disease cases reported in the US since 2013, with Neisseria meningitidis serogroup Y responsible for much of this recent increase.[7]
Most infections are sporadic, but about 5% of infections occur as part of outbreaks, caused predominantly by serogroups B, C, and Y.[1] The increasing incidence of serogroup W infections in the US, Europe, and Australia has been associated with a hypervirulent clonal strain.[9]
The highest rates of invasive infection are in children under age 5 years, especially those under age 1 year, with a second peak occurring in 11- to 24-year-olds and a third peak in people age >65 years.[10] Infections in infants and children ages 1-5 years are predominantly caused by serogroup B.[10]
Risk factors
Bactericidal serum and mucosal antibodies elicited by nasopharyngeal colonization with both Neisseria meningitidis and other Neisseria species increase over the first decade of life. In the third trimester of pregnancy these protective antibodies are transmitted transplacentally from mother to fetus. The highest rates of infection occur in children under age 1 year, following the physiologic waning of this maternally derived antibody.[4][19] Increased exposure to meningococcal carriers is probably responsible for a second peak in invasive infections in older adolescents.[20][21]
Hereditary or acquired deficiencies of the common complement pathway components C3, properdin, Factor D, Factor H, or C5-C9 are associated with high rates of invasive meningococcal infection and chronic meningococcemia.[4][19] Serum from patients with these deficiencies kills bacteria poorly, implying that serum complement-dependent bactericidal activity is a critical host defense.
The prevalence of complement deficiency in patients with invasive meningococcal infections ranges from 0% to 25%, and is higher in patients with recurrent meningococcal infections and those with infections caused by unusual serogroups.[22]
There is an estimated 1000- to 2000-fold increase in the risk of meningococcal infection among patients taking eculizumab, even if vaccinated.[23] Experts believe that the use of ravulizumab also confers an increased risk of invasive infection.
Eculizumab and ravulizumab are complement inhibitors that may be used in the treatment of paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and generalized myasthenia gravis.
Opsonophagocytic antibodies directed against the meningococcal capsular polysaccharide and against other bacterial antigens contribute to bacterial killing. Patients with congenital or acquired hypogammaglobulinemia, IgG subclass deficiencies, or functional immunoglobulin deficiencies are more susceptible to meningococcal infections, although rates of meningococcal infection in these patients are not as high as those of Streptococcus pneumoniae or Haemophilus influenzae.
People with HIV infection, in particular those with a low CD4 count or high viral load, are at increased risk of meningococcal disease.[24][25][26][27] In the US, the meningococcal serogroup ACWY vaccination is recommended in all patients with HIV over the age of 2 months, regardless of CD4 count.[20]
People with anatomic or functional hyposplenia are at increased risk of severe meningococcal infections, although the risk is not as great as that for Streptococcus pneumoniae infections.[28]
College students in the US and UK are at significantly higher risk for meningococcal infection than similarly aged peers who do not attend college.[27][29][30] Rates in first-year students, and particularly those living in dormitories, are 2- to 5-fold higher than in other students.[4][31] This is presumably related to a rapid increase in rates of meningococcal colonization during the first year of college.[21]
Over 95% of meningococcal infections in the US are sporadic. However, secondary cases may occur in contacts of patients with meningococcal infections.[32] Household contacts of people with meningococcal infection have infection rates ranging from 0.25% to 3%.[12] Contacts in schools and the workplace have a lower risk of infection (0.04% to 2.5%), with the highest rates in adolescents and people living or working in crowded conditions. Most secondary cases are diagnosed within 2 weeks of the index case. Outbreaks do occur within certain communities: for example, among gay and bisexual men in Melbourne, Australia in 2017, and in Florida in 2022.[33][34] People who are in a community affected by an outbreak are recommended to get vaccinated or receive booster vaccinations, depending on their individual risk factors and vaccination status.[20][35]
Household crowding is a risk factor for invasive meningococcal infection in children and adolescents, likely because living close to others facilitates the transmission of bacteria between household members.[20]
Serogroups A and C meningococcal infections are hyperendemic in the "sub-Saharan meningitis belt" extending from Senegal to Ethiopia, especially in the December-to-June dry season. During epidemics, attack rates may be as high as 1000 in 100,000 people.[36] Epidemics caused by W-135 and Y strains have occurred in several African countries, and serogroup A strain epidemics have occurred in India.[37] Travelers to these regions have increased rates of meningococcal disease. Infections have also been reported in participants in the Hajj pilgrimage to Saudi Arabia, and their household contacts.
Clinical microbiologists who have occupational exposure to Neisseria meningitidis are at increased risk of infection.[20][38] In many cases, these people have reported activities that were likely to have exposed them to infectious droplets or aerosols, or had confirmed exposure in the form of handling a confirmed N meningitidis isolate or specimen in the 14 days prior to symptom onset.[38]
Both smoking and passive exposure to tobacco smoke are risk factors for meningococcal carriage and invasive meningococcal disease.[20][27][39] Tobacco smoke impairs physical barriers to bacterial colonization, such as ciliary function and local cellular immune responses. It is toxic to respiratory epithelial cells, and bacteria may be better able to colonize and invade damaged respiratory epithelium.
People moving to a new living environment, particularly into a closed or semiclosed community such as a residential school, college dormitory, or military facility, have increased rates of meningococcal infection. Meningococcal carriage rates are high or increase rapidly in the first weeks of residence and are frequently sustained at elevated levels. The elevated risk of disease in these environments is likely related to higher rates of colonization in susceptible people.
Up to 50% of people with invasive meningococcal infections have had recent symptoms of an upper respiratory infection, and many have identifiable respiratory copathogens.[40][41] Respiratory pathogens may promote bacterial colonization by impairing local immunity or facilitating bacterial invasion. Coughing and sneezing may promote the transmission of Neisseria meningitidis to close contacts.
In adolescents and young adults, a risk factor for meningococcal disease is intimate kissing.[42] Smoking is a strong confounder in many studies.
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