Meningococcal Meningitis

Meningococcal meningitis (International Classification of Disease-9 [ICD-9] code: 036.0) 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.[4] 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.

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.

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.[5, 6]

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%.

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.

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.[7]

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%.[8]

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.[9]

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.[10]

For patient education information, see the Brain and Nervous System Center, as well as Meningitis in Adults and Meningitis in Children.

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.[3]

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.[9]

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)[12] may be used to complement standard laboratory procedures for the diagnosis of meningococcal meningitis.[13] The IS1106 PCR is a rapid and sensitive test for confirmation of the diagnosis; its sensitivity is not affected by prior antibiotic treatment.[14] PCR of the nspA gene was also reported to be a fast diagnostic test.[15]

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.

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.

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.

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.

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.[16]

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.[17] Current meningococcal vaccines are indicated for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis. MenHibrix, a combination vaccine, is a 4-dose sequence approved for use in children as young as 6 weeks old and is indicated for active immunity against invasive disease caused by Neisseria meningitides serogroups C and Y, and Haemophilus influenzae type b.

In October 2014, the FDA approved the first meningococcal vaccine for serogroup B (Trumenba) under the breakthrough therapy designation and accelerated approval regulatory pathways. Recent outbreaks of serogroup B meningococcal disease on a few college campuses have heightened concerns for this potentially deadly disease.

Approval was based on 3 randomized trials conducted in the United States and Europe in about 2800 adolescents. Among participants who were given 3 doses of the vaccine, 82% developed antibodies against 4 different N meningitidis serogroup B strains representative of those that cause serogroup B meningococcal disease in the United States compared with less than 1% before vaccination.[18]

In January 2015, a second meningococcal serogroup B vaccine was approved (Bexsero).[26]

According to the Centers for Disease Control and Prevention, in 2012, approximately 500 cases of meningococcal disease were reported; of those, 160 resulted from serogroup B.

Epidemics usually spread rapidly to a peak within weeks but may last for several months in the absence of vaccination.

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.[19] The vaccine is also recommended for adults and children at high risk (aged 2 months or older).[20, 21] 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.[22]

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.[23]

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.

Inpatient

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.[10]

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.

Class Summary

Penicillin is the drug of choice for the treatment of meningococcal meningitis and septicemia. Chemoprophylactic antimicrobials most commonly used to eradicate meningococci include rifampin, quinolones (eg, ciprofloxacin), ceftriaxone. Also included in this class are minocycline and spiramycin.

Ciprofloxacin (Cipro)

A single dose (500 mg) of ciprofloxacin may be effective for the eradication of meningococcal carriage in adults. This agent is for chemoprophylaxis only.

Penicillin G (Pfizerpen)

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.

Ceftriaxone (Rocephin)

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.

Rifampin (Rifadin, Rimactane)

Rifampin inhibits DNA-dependent bacteria, but not mammalian, RNA polymerase. This drug is for chemoprophylaxis only.

Chloramphenicol

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.

Minocycline (Minocin, Dynacin)

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.

Spiramycin

Spiramycin is a macrolide antibiotic that is used as a chemoprophylactic antimicrobial to eradicate meningococci. Spiramycin inhibits the growth of susceptible organisms. It is currently not available in the United States.

Class Summary

Meningococcal vaccines may be used to prevent and control outbreaks of serogroup C meningococcal disease according to CDC guidelines. They induce the formation of bactericidal antibodies to meningococcal antigens. They are used for active immunization against invasive meningococcal disease caused by inclusive serogroups.

Menactra is used for active immunization for persons aged 2-55 years for the prevention of invasive meningococcal disease. Menomune is approved for use in persons of aged 2 years and older and is the preferred vaccine for aged 56 years or older. Menveo is approved in persons aged 9 months to 55 years. A combination vaccine (MenHibrix) is also available. These vaccines do not prevent N meningitidis serogroup B infections.

In October 2014, the FDA approved the first vaccine for active immunization to prevent invasive meningococcal disease caused by N meningitidis serogroup B in individuals aged 10 through 25 years.[18] A second vaccine for serogroup B was approved in January 2015.[26]

Meningococcal A C Y and W-135 polysaccharide vaccine combined (Menomune A/C/Y/W-135)

Meningococcal vaccines may be used to prevent and control outbreaks of serogroup C meningococcal disease according to CDC guidelines. They induce the formation of bactericidal antibodies to meningococcal antigens. It is used for active immunization against invasive meningococcal disease caused by inclusive serogroups.

Meningococcal A C Y and W-135 diphtheria conjugate vaccine (Menactra, Menveo)

This vaccine is indicated for children as young as 9 months (Menactra) or 2 months (Menveo) and adults up to 55 years.

Meningococcal C and Y/haemophilus influenza type B vaccine (MenHibrix)

Menhibrix is a combination vaccine approved for use in children as young as 6 weeks old and is indicated to prevent invasive disease caused by Neisseria meningitides serogroups C and Y, and Haemophilus influenzae type b. Menhibrix was newly approved in 2012 and is a 4-dose sequence.

Meningococcal group B vaccine (Trumenba, Bexsero)

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 through 25 years.