Meningococcal meningitis has been recognized as a serious problem for almost 200 years. It was first identified definitely by Vieusseux in Geneva in 1805.
The causative organism, Neisseria meningitidis, is a gram-negative, aerobic, encapsulated diplococcus that grows best on enriched media, such as Mueller-Hinton or chocolate agar, at 37°C and in an atmosphere of 5-10% carbon dioxide.
Meningococcal disease still is associated with a high mortality rate and persistent neurologic defects, particularly among infants and young children.
The first successful treatment of meningitis with intravenous and intrathecal penicillin was reported in 1944, and the first clinical trials using high doses of intravenous penicillin as monotherapy for the treatment of meningitis were reported in 1950. Since then, penicillin has remained the drug of choice for the treatment of meningococcal meningitis.[1] However, current IDSA guidelines list ceftriaxone or cefotaxime as the drugs of choice.
The image below shows indications of increased intracranial pressure, an early complication of bacterial meningitis.
View Image
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead ....
Serogroups
Meningococci make up numerous serogroups that are based on the composition of their polysaccharide capsular antigens. They differ in their agglutination reactions to sera directed against polysaccharide antigens. At least 13 serogroups have been described: A, B, C, D, E, H, I, K, L, W-135, X, Y, and Z. Serogroups B and C have caused most cases of meningococcal meningitis in the United States since the end of World War II; before that, group A was more prevalent. More than 99% of meningococcal infections are caused by serogroups A, B, C, 29E, or W-135.
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 it is still the predominant cause of meningococcal meningitis in Africa and Asia.
Go to Haemophilus Meningitis, Meningitis, Staphylococcal Meningitis, Tuberculous Meningitis, Viral Meningitis, and Aseptic Meningitis for more complete information on these topics.
Individuals acquire meningococcal infections if they are exposed to virulent bacteria and have no protective bactericidal antibodies.
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).
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, the bacterium may be killed by bactericidal antibodies, complement, and phagocytic cells, or it may multiply, initiating the bacteremic phase. Organisms replicate rapidly.
Systemic disease appears with the development of meningococcemia and usually precedes meningitis by 24-48 hours. This can lead to systemic infection in the form of bacteremia, metastatic infection that commonly involves the meninges, or severe systemic infection with circulatory collapse and DIC. Meningococcemia leads to diffuse vascular injury, which is characterized by endothelial necrosis, intraluminal thrombosis, and perivascular hemorrhage.
Risk factors
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 predispose individuals to meningococcal disease.
Smoking and concurrent viral infection of the upper respiratory tract diminish the integrity of the respiratory mucosa and increase the likelihood of invasive disease. Crowding living conditions also facilitate disease spread, since individuals from different areas have different strains of meningococci.
Frequency and serogroup incidence in the United States
Since 1960, the incidence of meningococcal meningitis in the United States has been stable, at approximately 0.9-1.5 cases per 100,000 people per year. Most cases occur during winter and early spring.
Serogroups B and C have caused most cases of meningococcal meningitis in the United States since World War II. An increased frequency of serogroup B and Y meningococci has been noted since 1990. The frequency of localized outbreaks has increased since 1991.[2, 3]
Global disease distribution
As previously mentioned, 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 it 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 meningococcal meningitis pandemic that began in 1996 has resulted so far in approximately 300,000 cases being reported to the World Health Organization (WHO).
Morbidity and mortality in meningococcal meningitis
Morbidity and mortality rates from the disease remain high. Apart from epidemics, at least 1.2 million cases of bacterial meningitis are estimated to occur every year; 135,000 of them are fatal. Approximately 500,000 of these cases and 50,000 of the deaths are due to meningococci.
Early complications of bacterial meningitis include seizures, raised intracranial pressure (seen in the image below), cerebral venous thrombosis, sagittal sinus thrombosis, and hydrocephalus. The risk of cerebral herniation from acute meningitis is about 6-8%.
View Image
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead ....
In fulminant meningococcemia, severe disseminated intravascular coagulation (DIC) may develop, leading to hemorrhagic diathesis with bleeding into the lungs, urinary tract, and gastrointestinal tract. Ischemic complications of DIC also are common.
Infrequent suppurative complications include septic arthritis, purulent pericarditis, endophthalmitis, and pneumonia. Of survivors, 10% developed allergic complications manifested as cutaneous vasculitis or arthritis.
Late complications may include communicating hydrocephalus (which can present with gait difficulty, mental status changes, and incontinence) and hearing loss.[4]
In one study, 27% of survivors experienced 1 or more suppurative, allergic, or neurologic complications, including hearing loss, cutaneous vasculitis, and arthritis.
Hearing loss, noted in 9% of children, occurred significantly more often in patients with marked leukocytosis or leukopenia or with cerebrospinal fluid (CSF) leukocytosis greater than 10 X 109/L.
The Waterhouse-Friderichsen syndrome may develop in 10-20% of children with meningococcal infection. This syndrome is characterized by large petechial hemorrhages in the skin and mucous membranes, fever, septic shock, and DIC.
Even when the disease is diagnosed early and adequate therapy is instituted, the case-fatality rate in meningococcal meningitis ranges from 5-10%; it 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%.[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 neurologic sequelae.
A cohort study from Netherlands (the Meningitis Cohort Study) revealed a 7% mortality rate and an unfavorable outcome in 12% of the cases.[6]
Race predilection
In one study conducted in the United States, the incidence of meningococcal disease was slightly higher in African Americans (1.5 cases per 100,000 people) than in whites (1.1 cases per 100,000 people).
Sex predilection
In one study conducted in the United States, males accounted for 55% of total cases of meningococcal meningitis.
Age predilection
Meningococcal meningitis most commonly affects individuals aged between age 3 years and adolescence. It rarely occurs in individuals older than 50 years.
The prognosis for meningococcal meningitis is fair if the patient does not have focal neurologic deficits and is not stuporous or comatose. The prognosis for meningococcal disease is poor when the infection has a septicemic component. Most patients with meningococcal meningitis recover completely if appropriate antibiotic therapy is instituted promptly.
Thrombocytopenia, a lowered coagulation index, moderate anemia (hemoglobin < 11 g/dL), an obtunded mental state, and a history of convulsions were reported to be poor prognostic factors.
In one study, only anemia was correlated independently with fatality; the results suggested that anemia should be considered an important prognostic marker in the acute phase of meningococcal meningitis.
Advise any household contacts and close respiratory contacts that chemoprophylaxis agents are available to eliminate the carrier state and prevent the spread of infection.[7]
Meningococcal meningitis is characterized by acute onset of intense headache, fever, nausea, vomiting, photophobia, and stiff neck. Elderly patients are prone to have an altered mental state and a prolonged course with fever.
Lethargy or drowsiness in patients frequently is reported. Stupor or coma is less common. If coma is present, the prognosis is poor.
Patients also may complain of skin rash, which usually points to disease progression.
The clinical pattern of bacterial meningitis is quite different in young children. Bacterial meningitis in these patients usually presents as a subacute infection that progresses over several days.
Projectile vomiting may occur in children.
Seizures occur in 40% of children with meningitis, typically during the first few days. The majority of seizures have a focal onset.
In infants, the illness may have an insidious onset; stiff neck may be absent. In children, even when the combination of convulsive status epilepticus and fever is present, the classic signs and symptoms of acute bacterial meningitis may not be present.[8]
The Waterhouse-Friderichsen syndrome may develop in 10-20% of children with meningococcal infection. This syndrome is characterized by large petechial hemorrhages in the skin and mucous membranes, fever, septic shock, and DIC.
Neurologic signs of meningococcal meningitis include nuchal rigidity (eg, Kernig sign, Brudzinski sign), lethargy, delirium, coma, and convulsions.
Irritability is a common presenting feature in children.
However, in a 2008 published cohort study from Netherlands (the Meningitis Cohort Study), conducted in adult patients with meningococcal meningitis, only 70% of the patients had the classic triad of fever, neck stiffness, and change in mental status. If the presence of rash was added, 89% of the patients had 2 of the 4 features.[6]
Patients older than 30 years were noted to have petechiae (62%) less frequently than younger patients (81%).
A more severe, but less common form of meningococcal disease, is meningococcal septicemia, which is characterized by rapid circulatory collapse and a hemorrhagic rash.
A petechial or purpuric rash usually is found on the trunk, legs, mucous membranes, and conjunctivae. Occasionally, it is on the palms and soles. The rash may progress to purpura fulminans, when it usually is associated with multiorgan failure (ie, Waterhouse-Friderichsen syndrome). The petechial rash may be difficult to recognize in dark-skinned patients.
Laboratory examination of the cerebrospinal fluid (CSF) usually confirms the presence of meningitis.
In the US, a neuroimaging study (either MRI or CT scanning) prior to lumbar puncture is mandatory in all patients in whom meningitis is suspected. However, this rule is relaxed in several other countries (see CT scanning and MRI).
Typical CSF abnormalities in meningitis include the following:
Increased opening pressure (>180 mm water)
Pleocytosis of polymorphonuclear leukocytes (white blood cell [WBC] counts between 10 and 10,000 cells/µL, predominantly neutrophils)
Decreased glucose concentration (< 45 mg/dL)
Increased protein concentration (>45 mg/dL)
Gram stain and culture of CSF identify the etiologic organism, N meningitides. In bacterial meningitis, Gram stain is positive in 70-90% of untreated cases, and culture results are positive in as many as 80% of cases.
More specialized laboratory tests, which may include culture of CSF and blood specimens, are needed for identification of N meningitidis and the serogroup of meningococci, as well as for determining its susceptibility to antibiotics.
The polymerase chain reaction (PCR)[10] may be used to complement standard laboratory procedures for the diagnosis of meningococcal meningitis.[11] The IS1106 PCR is a rapid and sensitive test for confirmation of the diagnosis; its sensitivity is not affected by prior antibiotic treatment.[12] PCR of the nspA gene was also reported to be a fast diagnostic test.[13]
Head CT scan findings are usually normal but may reveal signs of intracranial hypertension, edema, and intracerebral hemorrhage. In several parts of the world, imaging is an important cause of delay of therapy. In the US, due to the large availability of brain imaging, the performance of a head CT scan is mandatory. In other countries, this rule is relaxed, and indications for performing CT scanning prior to lumbar puncture include altered level of consciousness, papilledema, focal neurological deficits, and/or focal or generalized seizure activity.
The image below depicts intracerebral hemorrhage foci and diffuse edema in a patient with meningitis.
View Image
Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique ....
MRI with contrast is preferred to CT scanning, because MRI better demonstrates meningeal lesions, cerebral edema, and cerebral ischemia. T1 may show obliterated cisterns. Contrast enhances the cisterns, and extension of enhancing subarachnoid exudate deep into the sulci may be seen in severe cases.
Strokes can be seen with the development of vasculitis and cerebritis. CNS complications that can be visualized with MRI include hydrocephalus, aqueductal obstruction, ventriculitis (especially in neonates), choroid plexitis, subdural effusion, and empyema.
View Image
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead ....
View Image
Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique ....
During the first few days, the subarachnoid and ventricular exudate contains large numbers of neutrophils and necrotic debris. Intracellular and extracellular bacteria can be demonstrated. The exudate extends along the perivascular spaces into the cortex and cerebral cortex. Purulent material usually is observed in the choroid plexus. With time, the number of mononuclear leukocytes increases, and they predominate by the end of the first week. Fibroblasts also proliferate.
Inflammatory cells infiltrate leptomeningeal and cortical arteries and veins and accumulate in the intima. Thrombosis of small vessels leads to infarction. This pattern is common in autopsied cases.
An electroencephalogram (EEG) study is sometimes useful to document irritable electrical patterns that may predispose the patient to seizures. Periodic complexes and periodic lateralizing epileptiform discharges (PLEDs) may be suggestive of encephalitis caused by herpes simplex virus.
Meningococcal disease is potentially fatal and always should be viewed as a medical emergency. Admission to a hospital is necessary. To prevent serious neurologic morbidity and death, prompt institution of antibiotic therapy is essential when the diagnosis of bacterial meningitis is suspected.
Surgical interventions may be necessary for the management of complications, such as subdural effusions, empyema, and hydrocephalus.
Institute antimicrobial therapy as soon as possible after the lumbar puncture is performed.
Long delays may occur in the emergency department before initiation of antibiotics in patients with suspected bacterial meningitis. In general, these delays appear to be physician generated and, to a great extent, potentially avoidable.[14]
A study has suggested that, at least in children, CSF sterilization may occur more rapidly after initiation of parenteral antibiotics than previously suggested, with complete sterilization of meningococcus within 2 hours and the beginning of sterilization of pneumococcus by 4 hours.
Standard empirical therapy
At presentation, meningitis due to N meningitidis may be impossible to differentiate from other types of meningitis. Thus, empirical treatment with an antibiotic with effective CNS penetration should be based on age and underlying disease status, since delay in treatment is associated with adverse clinical outcome.
Initial empirical therapy until the etiology is established should include dexamethasone, a third-generation cephalosporin (eg, ceftriaxone, cefotaxime), and vancomycin. Acyclovir should be considered according to the results of the initial cerebrospinal fluid (CSF) evaluation. Doxycycline should also be added during tick season in endemic areas. A 7-day course of intravenous ceftriaxone or penicillin is adequate for uncomplicated meningococcal meningitis.
If imaging studies are indicated before lumbar puncture, draw blood for culture and begin administration of empiric antibiotics. Administration of empiric antibiotics is unlikely to decrease diagnostic sensitivity if CSF is tested for bacterial antigens early in the course of the illness.
Treatment following diagnosis
Once an accurate diagnosis of meningococcal meningitis is established, appropriate changes can be made. Currently, a third-generation cephalosporin (ceftriaxone or cefotaxime) is the drug of choice for the treatment of meningococcal meningitis and septicemia. Penicillin G, ampicillin, chloramphenicol, fluoroquinolone, and aztreonam are alternatives therapies (IDSA guidelines).
The use of dexamethasone in the management of bacterial meningitis in adults remains controversial. It may be used in children, especially in those with meningitis caused by Haemophilus influenzae. In adults with suspected bacterial meningitis, especially in high-risk cases, the adjunctive use of dexamethasone may be beneficial.
Person-to-person transmission can be interrupted by chemoprophylaxis, which eradicates the asymptomatic nasopharyngeal carrier state.
Deterrence and prevention of meningococcal meningitis can be achieved by either immunoprophylaxis or chemoprophylaxis. Rifampin, quinolones, and ceftriaxone are the antimicrobials that are used to eradicate meningococci from the nasopharynx.
Immunoprophylaxis
Vaccination is used for close contacts of patients with meningococcal disease due to A, C, Y, or W135 serogroups, to prevent secondary cases.[15] Current meningococcal vaccines are indicated for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis.
In October 2024, the Advisory Committee on Immunization Practices (ACIP) approved the Recommended Immunization Schedule for Adults Ages 19 Years or Older, United States, 2025.For the MenACWY vaccine, booster doses are advised following the initial series. The updated guidelines now include the revised vaccination schedule for MenB, Bexsero. For routine vaccination, it is recommended that healthy individuals aged 16–23 years receive a 2-dose series, with doses administered 6 months apart, based on shared clinical decision-making. Adults at increased risk for serogroup B meningococcal disease should receive a 3-dose series at intervals of 0, 1–2, and 6 months. Furthermore, the new recommendations for the use of the MenB vaccine during pregnancy suggest postponing vaccination until after pregnancy, due to insufficient safety data for pregnant individuals.
During their October 2024 session, the Advisory Committee on Immunization Practices (ACIP) endorsed the Recommended Immunization Schedule for Children and Adolescents up to 18 Years Old in the United States for the year 2025.[16]
The "Routine Vaccination" and "Special Situations" sections have been updated to incorporate the new Bexsero vaccination schedule. For healthy individuals aged 16–23 years, a two-dose series spaced 6 months apart is advised, contingent upon shared clinical decision-making. For children and adolescents aged 10 years and older who are at increased risk for serogroup B meningococcal disease, a three-dose series at 0, 1–2, and 6-month intervals is recommended.[16]
In 2014, the FDA approved Trumenba, the first vaccine for meningococcal serogroup B, following outbreaks on college campuses. This approval was based on three randomized trials in the United States and Europe with about 2800 adolescents, showing 82% developed antibodies against four strains of serogroup B.[17]
In 2015, the FDA approved a second serogroup B vaccine, Bexsero.[18]
In 2023, the FDA approved Penmenvy, the first pentavalent meningococcal vaccine targeting serogroups A, B, C, W, and Y. This approval came from a trial with 2341 participants aged 10–24 years, where Penmenvy demonstrated noninferiority to existing vaccines, Trumenba and Menveo, in preventing disease caused by these serogroups.[19]
In 2025, the FDA approved Penmenvy, the second meningococcal pentavalent vaccine for adolescents and young adults aged 10–25 years.[20, 21]
Mass immunization of selected communities, using polyvalent A and C polysaccharide vaccine, is a useful control measure.
Vaccines against meningococcus A, C, W, and Y are available. ACIP guidelines include a recommendation for primary immunization for children aged 11-12 years, with a booster dose at age 16 years.[22] The vaccine is also recommended for adults and children at high risk (aged 2 months or older).[23, 24] High-risk persons include military recruits, contacts to index cases, individuals travelling to areas of high incidence or areas affected by outbreaks, patients with asplenia, adolescents with HIV infection, and persons with terminal complement disorders. Serogroup B vaccine is indicated as a 3-dose series in adolescents and young adults aged 10 through 25 years. College students also benefit from vaccination.
Chemoprophylaxis
In general, chemoprophylaxis is not recommended during epidemics because of multiple sources of exposure and prolonged risk of exposure. Logistic problems and high cost also make this an impractical alternative.[25]
Chemoprophylaxis can be considered for people in close contact with patients in an endemic situation. Ciprofloxacin 500 mg in a single dose is probably the easiest option in adults. Children could receive either a single IM injection of ceftriaxone or 4 oral doses of rifampin over 2 days, according to body weight.
Antimicrobials commonly used for chemoprophylaxis are rifampin, ciprofloxacin, ceftriaxone, minocycline, and spiramycin.
When oral rifampin (4 doses in 2 d) was compared with a single IM dose of ceftriaxone for prophylaxis, follow-up cultures indicated that ceftriaxone was significantly more effective. Ceftriaxone may provide an effective alternative to rifampin for prophylaxis in people in close contact with patients with meningococcal meningitis.[26]
Oily chloramphenicol may be the drug of choice in areas with limited health facilities, because a single dose of the long-acting form has been shown to be effective.
Sometimes, an alternative to chemoprophylaxis may be protective chemotherapy that can prevent the development of meningitis in individuals incubating the disease.
Complete appropriate antimicrobial therapy course. Observe the patient for any complications or neurological sequelae.
Outpatient
Advise any household contacts and close respiratory contacts that chemoprophylaxis agents are available to eliminate the carrier state and prevent the spread of infection.[7]
Observe patients for any late complication or neurologic sequelae.
To prevent neurologic damage or death, it is essential to promptly institute empirical therapy with an antibiotic that has effective CNS penetration, is essential when the diagnosis of bacterial meningitis is suspected. Such treatment with should be based on age and underlying disease status, since delay in treatment is associated with adverse clinical outcome.
Clinical Context:
This agent is a third-generation cephalosporin with broad-spectrum, gram-negative activity. It has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms.
Clinical Context:
Chloramphenicol acts by inhibiting bacterial protein synthesis. It binds reversibly to the 50S subunit of bacterial 70S ribosome and prevents attachment of the amino acid–containing end of the aminoacyl-tran to the acceptor site on the ribosome. It is active in vitro against a wide variety of bacteria, including gram-positive, gram-negative, aerobic, and anaerobic organisms. Oily chloramphenicol may be the drug of choice in areas with limited health facilities, because a single dose of the long-acting form has been shown to be effective.
Clinical Context:
A single dose (500 mg) of ciprofloxacin may be effective for the eradication of meningococcal carriage in adults. This agent is for chemoprophylaxis only.
Clinical Context:
Minocycline is a member of the tetracycline class of antimicrobial agents. It is a broad-spectrum agent that inhibits susceptible organisms by blocking their protein synthesis. Although an oral form of the drug has been approved for chemoprophylactic use to eradicate the meningococcal carrier state, its use for these purposes was associated with a high incidence of general and gastrointestinal symptoms. The use of minocycline should be reserved for situations in which the risk of meningococcal meningitis is high.
Clinical Context:
Patients in whom meningococcal disease is suspected should receive a high dose of this drug, which interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.
Clinical Context:
First pentavalent vaccine approved for meningococcal groups A, B, C, W and Y pentavalent vaccine (Penbraya). Provides coverage against the most common serogroups causing meningococcal disease in adolescents and young adults aged 10–25 years.
Clinical Context:
Indicated for prevention of invasive meningococcal disease caused by Neisseria meningitidis serogroups A, C, Y, and W-135 in persons aged ≥ 2 years.
Clinical Context:
The vaccine is administered as a 3-dose series at months 0, 2, and 6 (Trumenba) or a 2-dose series given at least 1 month apart (Bexsero). It induces production of bactericidal antibodies directed against the capsular polysaccharides of serogroup B. It is indicated for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis serogroup B in individuals aged 10–25 years.
What is the prognosis of meningococcal meningitis?What are the signs and symptoms of meningococcal meningitis?What are the signs and symptoms of meningococcal meningitis in young children?How is a diagnosis of meningococcal meningitis confirmed?What is the role of lab testing in the diagnosis of meningococcal meningitis?What is the role of imaging studies in the diagnosis of meningococcal meningitis?What is the role of electroencephalography in the diagnosis of meningococcal meningitis?What is the role of antibiotic therapy in the treatment of meningococcal meningitis?Which medications are used in initial empiric therapy of meningococcal meningitis?Which medications are used in the treatment of confirmed meningococcal meningitis?How is meningococcal meningitis prevented?What is meningococcal meningitis?What are serogroups of meningococci that cause meningococcal meningitis?What causes meningococcal meningitis?What are the risk factors for meningococcal meningitis?What is the incidence of meningococcal meningitis in the US?What is the global incidence of meningococcal meningitis?What is the morbidity and mortality of meningococcal meningitis?What are the race predilections of meningococcal meningitis?What are the sexual predilections of meningococcal meningitis?Which age groups are at highest risk for meningococcal meningitis?What is the prognosis of meningococcal meningitis?What is included in patient education about meningococcal meningitis?What are the signs and symptoms of meningococcal meningitis?Which physical findings are characteristic of meningococcal meningitis?Which conditions should be included in the differential diagnoses of meningococcal meningitis?What are the differential diagnoses for Meningococcal Meningitis?How is a diagnosis of meningococcal meningitis confirmed?What is the role of CSF analysis in the diagnosis of meningococcal meningitis?What is the role of PCR in the workup of meningococcal meningitis?What is the role of CT scanning in the workup of meningococcal meningitis?What is the role of MRI in the workup of meningococcal meningitis?Which histologic findings are characteristic of meningococcal meningitis?What are other tests used in the workup of meningococcal meningitis?How is meningococcal meningitis treated?What is the role of pharmacologic therapy in the treatment of meningococcal meningitis?How is meningococcal meningitis prevented?What is the efficacy of vaccination against meningococcal meningitis?What is the role of chemoprophylaxis for prevention of meningococcal meningitis?What is included in inpatient care of meningococcal meningitis?What is included in long-term monitoring following treatment of meningococcal meningitis?What is the role of empiric therapy in the treatment of meningococcal meningitis?Which medications in the drug class Vaccines are used in the treatment of Meningococcal Meningitis?Which medications in the drug class Antibiotics are used in the treatment of Meningococcal Meningitis?
Francisco de Assis Aquino Gondim, MD, PhD, MSc, FAAN, Professor Adjunto of Neurology and Clinical Skills, Department of Internal Medicine, Universidade Federal do Ceará, Brazil
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Consultant for Pfizer, PTC Therapeutics and Alnylam<br/>Serve(d) as a speaker or a member of a speakers bureau for: Speaker for Shire, PTC Therapeutics and BSL Beringer<br/>Received travel grants from for: Aché, Biogen, Genzyme, Ipsen, Novartis, Baxter, Teva, Pfizer.
Coauthor(s)
Manish K Singh, MD, Director - Jersey Institute of Neuroscience ,
Cape may Court House, NJ.
Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Florian P Thomas, MD, PhD, MA, MS, Chair, Neuroscience Institute and Department of Neurology, Director, Hereditary Neuropathy Center, Co-Director, Center for Memory Loss and Brain Health, Co-Director, ALS Center, Hackensack University Medical Center; Associate Dean of Faculty, Founding Chair and Professor, Department of Neurology, Hackensack Meridian School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM, Adjunct Associate Professor of Neurology, University of Missouri-Columbia School of Medicine; Medical Director of St Mary's Stroke Program, SSM Neurosciences Institute, SSM Health
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbie and Pfizer.
Additional Contributors
Norman C Reynolds, Jr, MD, Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Sidney E Croul, MD, to the development and writing of the source article.
Issa AN, Wodi AP, Moser CA, Cineas S. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger — United States, 2025. MMWR. January 16, 2025. 74(2):27-29.
FDA News Release: First vaccine approved by FDA to prevent serogroup B Meningococcal disease. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm420998.htm. Accessed: October 29, 2014.
FDA News Release. FDA approves a second vaccine to prevent serogroup B meningococcal disease. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm431370.htm. Accessed: January 23, 2015.
MenABCWY Noninferiority Study in Healthy Participants ≥10 to https://www.clinicaltrials.gov/study/NCT04440163https://www.clinicaltrials.gov/study/NCT04440163</a>. 2023 Apr 18; Accessed: October 24, 2023.
Novartis Vaccines. FDA expands age indication for Menveo®, first and only quadrivalent meningococcal vaccine for infants as young as 2 months of age. Available at http://www.novartisvaccines.com/newsroom/media-releases/2013/US_Menveo_Infant_FDA_Approval_Press_Release_US.pdf. Accessed: August 7, 2013.
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead shows small intracerebral hemorrhage foci on the right temporal lobe, and the curved arrow shows the effect of increased intracranial pressure on the cerebellum.
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead shows small intracerebral hemorrhage foci on the right temporal lobe, and the curved arrow shows the effect of increased intracranial pressure on the cerebellum.
Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique closed arrow). The black arrow head on the left shows soft tissue edema.
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead shows small intracerebral hemorrhage foci on the right temporal lobe, and the curved arrow shows the effect of increased intracranial pressure on the cerebellum.
Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique closed arrow). The black arrow head on the left shows soft tissue edema.
Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead shows small intracerebral hemorrhage foci on the right temporal lobe, and the curved arrow shows the effect of increased intracranial pressure on the cerebellum.
Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique closed arrow). The black arrow head on the left shows soft tissue edema.
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